Why do fruits rot?

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Why do fruits rot?

 
 

Why do fruits rot?

#1  Postby quas » Jan 09, 2012 2:05 pm

As fruit ripens, starch breaks down to sugar. Sugar, being hygroscopic, is a good preservative. So how did the fruit rot?
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Re: Why do fruits rot?

#2  Postby mattwilson » Jan 09, 2012 2:09 pm

Because bacteria just fucking love sugar om nom nom
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Re: Why do fruits rot?

#3  Postby quas » Jan 09, 2012 2:41 pm

And the bacteria can thrive without water?
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Re: Why do fruits rot?

#4  Postby Zwaarddijk » Jan 09, 2012 2:49 pm

quas wrote:And the bacteria can thrive without water?

fruits normally are dry?
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Re: Why do fruits rot?

#5  Postby mattwilson » Jan 09, 2012 2:50 pm

You just said, it's hygroscopic so there's water there for the bacteria... mmm lovely sugar and water om nom nom
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Re: Why do fruits rot?

#6  Postby Matt_B » Jan 09, 2012 3:20 pm

Dried fruit does tend to keep rather longer than fresh fruit, so there's your answer.
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Re: Why do fruits rot?

#7  Postby chairman bill » Jan 09, 2012 3:26 pm

There's also the amount of sugar in relation to other substances. If you soaked the fruit in syrup, so significantly raising the sugar content, you'd reduce the likelihood of rotting. Let the fruit then dry, and the process can be made to gradually increase the amount of sugar to about 80% by weight, by soaking in ever-increasing concentrations of sugar in the syrup, so that eventually you get crystallised/candied fruit. Lots of sugar, bugger all water, and it keeps & keeps.
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Re: Why do fruits rot?

#8  Postby lordshipmayhem » Jan 09, 2012 3:32 pm

chairman bill wrote:eventually you get crystallised/candied fruit. Lots of sugar, bugger all water, and it keeps & keeps.

Until the kids discover your stash... nomnomnom
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Re: Why do fruits rot?

#9  Postby Sityl » Jan 09, 2012 3:33 pm

In terms of evolution, it rots because a) the bacteria get free food (om nom nom) and b) what's left = great fertilizer for seeds!
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Re: Why do fruits rot?

#10  Postby quas » Jan 10, 2012 1:51 am

Is it the bacteria or the enzymes that cause the rotting? I mean, supposing that the bacteria is deactivated in a relatively dry environment, can the enzymes still cause the fruit to rot?
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Re: Why do fruits rot?

#11  Postby nygreenguy » Jan 10, 2012 2:34 am

quas wrote:Is it the bacteria or the enzymes that cause the rotting? I mean, supposing that the bacteria is deactivated in a relatively dry environment, can the enzymes still cause the fruit to rot?


Mostly the bacteria, but the lack of "life" in the fruit will cause some structural degradation.

If enzymes alone caused fruit to rot, we wouldnt be able to preserve fruit without degrading all the enzymes which would make the fruit pretty un-yummy.
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Re: Why do fruits rot?

#12  Postby Gallstones » Jan 10, 2012 3:12 am

Everything rots eventually.
Saprophytes evolved mechanisms to overcome the inhibitions to easy decomp.
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Re: Why do fruits rot?

#13  Postby Berthold » Jan 13, 2012 1:59 am

Sityl wrote:b) what's left = great fertilizer for seeds!

Only if the primary function of the fruit flesh (getting eaten by animals that afterwards walk around and poop the seeds) is not fulfilled; also, the proverbial apple that falls close to the tree does not have overly great opportunities to grow big trees from its seeds.
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Re: Why do fruits rot?

#14  Postby Horwood Beer-Master » Jan 13, 2012 10:12 am

quas wrote:Is it the bacteria or the enzymes that cause the rotting? I mean, supposing that the bacteria is deactivated in a relatively dry environment, can the enzymes still cause the fruit to rot?

As others have already pointed out - a rotting fruit is not (normally) a dry environment. Where fruits are dried, they tend not to rot (or at least decomp is drastically slowed).
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Re: Why do fruits rot?

#15  Postby DavidMcC » Feb 08, 2012 4:10 pm

Perhaps it's obvious, but succulent fruits eventually fall to the ground as well as rot, if they do not get eaten as "intended" by the plant. This obviously helps return nutrients to the soil.
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Re: Why do fruits rot?

#16  Postby DavidMcC » Feb 09, 2012 9:57 am

... Also, the weakening of the stem that assists the eating of them by animals also helps with the falling stage for those not eaten.
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Re: Why do fruits rot?

#17  Postby Calilasseia » Feb 09, 2012 11:46 am

Some time ago over at RDF, I put forward the suggestion that oxidation was the 'kick start' for decomposition when dealing with a paper on experimental taphonomy, in relation to sea urchin embryos. When I delved into that paper, the authors revealed that the native proteases in the cells initiated the decomposition process instead.

Oh look, I archived the post on my hard drive. I'll reproduce it here. The original post was devoted to refuting some more wankery from Arsewater in Genesis about the formation of fossils, but the details may be applicable to the matter of fruit decomposition. The post in question reads as follows:


Experimental Taphonomy Refutes Creationist Apologetic Bullshit About Fossils

And here is the relevant scientific paper covering the experimental work ...

Experimental Taphonomy Shows The Feasibility Of Fossil Embryos by Elizabeth C. Raff, Jeffrey T. Villinski, F. Rudolf Turner, Philip C. J. Donoghue and Rudolf A. Raff, Proceedings of the National Academy of Sciences of the USA, 103(15): 5846-5851 (11th April 2006)

Let's take a look at what this paper says shall we?

Raff et al, 2006 wrote:The recent discovery of apparent fossils of embryos contemporaneous with the earliest animal remains may provide vital insights into the metazoan radiation. However, although the putative fossil remains are similar to modern marine animal embryos or larvae, their simple geometric forms also resemble other organic and inorganic structures. The potential for fossilization of animals at such developmental stages and the taphonomic processes that might affect preservation before mineralization have not been examined. Here, we report experimental taphonomy of marine embryos and larvae similar in size and inferred cleavage mode to presumptive fossil embryos. Under conditions that prevent autolysis, embryos within the fertilization envelope can be preserved with good morphology for sufficiently long periods for mineralization to occur. The reported fossil record exhibits size bias, but we show that embryo size is unlikely to be a major factor in preservation. Under some conditions of death, fossilized remains will not accurately reflect the cell structure of the living organism. Although embryos within the fertilization envelope have high preservation potential, primary larvae have negligible preservation potential. Thus the paleo-embryological record may have strong biases on developmental stages preserved. Our data provide a predictive basis for interpreting the fossil record to unravel the evolution of ontogeny in the origin of metazoans.


So, what the scientists did in this paper, was create experimental conditions to test whether or not it was possible for embryonic aquatic organisms of the relevant phyla to be preserved long enough for mineralisation processes to begin, by devising appropriate conditions in the laboratory. In particular, they devised a series of conditions to prevent a process known as autolysis, namely tissues breaking down due to spontaneous chemical reactions after death, usually the result of oxidation processes that result in a cascade of other chemical reactions between the oxidised constituents. Since oxidation is an important factor in autolysis, it was determined, courtesy of well understood chemistry, that an environment preventing autolysis would be strongly reducing in nature, and appropriate reducing agents exist in natural systems. One that is of particular importance is hydrogen sulphide, H2S, a gas that is produced by anaerobic bacteria among other sources (it is also a product of some volcanic emissions), and which is a well-known reducing agent in chemistry. The appearance of H2S in aquatic systems is well known to aquarists like myself, and occurs whenever "dead spots" appear in a substrate that are deprived of oxygen for some reason, one reason why undergravel filters became popular in aquaria to eliminate these "dead spots" and promote the flourishing of aerobic nitrifying bacteria that help maintain water quality in the medium term. I shall leave aside the different technologies used in marine reef aquaria to achieve a similar end result with respect to nitrification, as this is not relevant here, but the appearance of H2S in aquatic substrates is a familiar and well documented process, indeed quite a few ponds will liberate the foul-smelling gas if the substrate is disturbed.

Now, the material used as the reducing agent in this instance was somewhat different from H2S for safety reasons (hydrogen sulphide is a readily flammable gas, as well as being as toxic as cyanide if inhaled in quantity, leading to death by respiratory arrest). However, a reducing agent possessing chemical properties as close to those of H2S as possible without the safety hazards was selected for the experiments. β-mercaptoethanol, HO-CH2-CH2-SH, which exhibits similar reducing chemistry, is also liquid at room temperature (thus vastly reducing the hazard level from inhalation) and readily soluble in water.

So, let's move on and continue with the paper.

Raff et al, 2006 wrote:Discovery of microfossils interpreted as metazoan embryos and larvae in rocks of Ediacaran and Cambrian age putatively coeval with the metazoan radiation (1–11) has the promise to provide direct insight into developmental mode in animal evolution. In contrast to the record for living metazoans, the Ediacaran and Cambrian record of fossilized embryos has been interpreted to represent only direct developing lecithotrophic forms. However, the available fossil record is biased and in different ways in different deposits (6, 12, 13). Putative fossil cleavage-stage embryos from the Ediacaran Doushantuo Formation are large in comparison with many modern embryos. Discussion to date has centered on the difficulty of distinguishing fossils of cleaving embryos from fossils of other multicellular forms, such as algae (5). Moreover, the validity of some putative fossils, particularly those interpreted as larval forms, has been questioned (2, 3, 5, 14). Whether primary larvae can be preserved as fossils has not been addressed.

Previous experimental studies of soft tissue mineralization showed that after introduction of an anaerobic bacterial community and sea floor sediment to shrimp carcasses, oxygen levels fell, sulfide levels rose, pH levels fell, and phosphatization of muscle tissue occurred within a month (15). A link was made between anaerobic decay and mineralization. Where oxygen is available, calcium carbonate deposition dominates, whereas in a closed system, calcium phosphate deposition can replicate soft tissues within 2 weeks (16, 17). Similar studies of embryos were not as successful at preserving cell structure. Experimental mineralization of lobster eggs in the presence of anaerobic sediments resulted in calcium carbonate deposition on the tough external egg envelope within 15–36 days, but no preservation or mineralization of the embryos within was observed (18). Anyone who works with marine embryos would consider preservation for sufficient time for mineralization via phosphatization unlikely, given the seeming fragility of such embryos. Freshly killed marine embryos in normal seawater decompose within a few hours. We carried out taphonomy experiments designed to uncover the impact of the mode of death and postdeath environment on the preservational potential of marine embryos and larvae.


So, prior to the work done by the authors of this paper, there have been prior experiments on the likely conditions required for mineralisation to begin, and a link between an anaerobic, reducing environment has already been established in experimental work on larger organisms. An anaerobic, reducing environment is associated with both preservation of soft tissues long enough for mineralisation to begin, and the onset of a process known as phosphatisation, whereby calcium phosphate begins to replace some of the soft tissue.

However, prior experiments to establish such conditions for embryonic material before this paper have been largely regarded as failures. Thus, the authors sought to determine what conditions would result in successful preservation of embryonic material, in order to obtain experimental evidence that embryos could fossilise under the appropriate conditions.

Moving on ...

Raff et al, 2006 wrote:The presumptive fossil cleavage embryos described to date are large in size (≅500 μm) and exhibit a covering that resembles a fertilization envelope and closely packed equal-sized cells resembling a pattern of cell division in which blastomere size decreases with increasing cell number, typical of cell division without cell growth in early embryos. We used the lecithotrophic Australian sea urchin Heliocidaris erythrogramma as a model in our decay experiments because its embryos exhibit a comparable suite of features (19, 20). Mineralization was not studied, but conditions consistent with phosphatization (15–18) were investigated.

We also studied the effects of preservation conditions on small, planktotrophic sea urchin embryos and larvae to determine whether size of embryos is a determining factor in preservability. If it was, the bias toward reports of large-sized embryos in the Precambrian and Cambrian record might reflect a preservation bias and not contemporaneous embryological diversity. Our results show that under some experimental circumstances compatible with natural conditions maintenance of marine embryos for time periods compatible with the authigenic replication of soft tissue can potentially occur, but for only a limited set of developmental stages.


So, what the authors of the paper decided to do, was select an organism whose embryos bore as much resemblance to the fossils as possible, determined on the basis of morphological characteristics, induce the organisms to breed, then test under what conditions the embryonic offspring underwent the appropriate processes. When this was done, it was determined that in situ phosphatisation could occur, but not for every possible embryonic developmental stage.

Moving on again ...

Raff et al, 2006 wrote:Results
Effect of Death and Postdeath Conditions on Embryo Morphology.


We compared normal cleavage stage H. erythrogramma embryos (Fig. 1 A–D) with embryos subjected to various experimental treatments (Fig. 1 E–L). Scanning electron microscopic images of H. erythrogramma embryos in Fig. 1 bear a striking resemblance in general appearance and size to putative fossil cleavage embryos described from Ediacaran and Cambrian rocks (1, 6, 13, 14). The rate of killing was important. Embryos killed rapidly (Fig. 1 E–I) retained blastomere numbers and arrangements of the time of death. Rapid death allowed retention of normal morphology, except if by lowered salinity, which affected cell shape. In hypotonic seawater, two-cell embryos retained uniform blastomere configuration, but the cells swelled to fill the fertilization envelope, producing a distinct morphology that if fossilized might be interpreted as an embryo of a different taxon (Fig. 1G). When embryos died slowly, individual blastomeres displayed differential cleavage patterns and timing of arrest, yielding abnormal, nonuniform morphologies (Fig. 1 J and K). The aberrant cleavage patterns resulting from slow death resembled those in polyspermic embryos (Fig. 1L).

Extended Preservation of Cleavage-Stage Embryos in Strong Reducing Conditions.

Because in situ mineralization is associated with anoxic reducing environments (15–18), we examined H. erythrogramma embryos placed into comparably strong reducing conditions, either directly or after they had been killed by other treatments. In a reducing environment, cleavage-stage embryos exhibited striking potential for extended preservation with normal morphology (Figs. 1 E and F and 2 A–C). Examination of killed embryos returned to normal seawater showed that the inactivation of proteins that occurs under reducing conditions is a necessary correlate of preservation. For cleavage-stage embryos, the presence of the fertilization envelope provides a protective barrier both from physical damage and external decay processes, including bacterial action and protist predation. Within an intact fertilization envelope, the pericellular space provides an apparently sterile medium surrounding the embryo (21, 22). Nonetheless, in normal seawater, dead embryos rapidly degrade through the process of autolysis. This internal cell destruction is caused by the action of endogenous proteases and other lytic enzymes, resulting in loss of cell boundaries, swelling, fusion of lipid droplets, and finally disintegration (Fig. 2D). Autolysis of dead cleavage-stage embryos was well underway by 18 h postdeath. To be fossilized with good morphology, embryos would need to encounter conditions that block autolysis, such as a reducing environment, very soon after death.


So, cleavage-stage embryos exhibit significant autolysis (initial decay processes) just 18 hours after death under normal seawater conditions. The question is, does a reducing environment halt this? Let us move on ...

Raff et al, 2006 wrote:Autolysis was prevented experimentally in the reducing conditions produced by the addition of 100 mM β-mercaptoethanol (β-ME) to normal seawater (Figs. 1 E and F and 2 A–C). In this environment, protein disulfide bonds were reduced and enzymes were inactivated; embryos were still intact 3 weeks after their killing, when the experiment was concluded. If embryos were returned from reducing conditions to normal seawater, fertilization envelopes degenerated, and the embryos were subject to normal decay processes, including bacterial action and attack by hypotrichous ciliates (Fig. 2E). Because of the extreme toxicity and difficulty of working with H2S, we used seawater containing 100 mM β-ME as a stand-in for the high H2S levels that may be present under anoxic conditions on the sea floor. Concentrations of H2S up to 30–100 mM have been reported from some modern marine environments (23, 24). At least some deposits containing Ediacaran and Cambrian fossil embryos are rich in pyrite, including the Doushantuo phosphorite, indicating substantial H2S levels at the time of fossilization (10, 25). H2S has similar reducing potential as thiols (26–29), and at the reported concentrations should effectively reduce protein S-S bonds in embryos that fall into such a sea-floor environment. The key is an environment in which autolytic processes are inactivated.


So, this paragraph confirms my earlier reporting about the reducing properties of H2S and its prevalence in certain aquatic environments (in the case of the use of H2S as a reducing agent, any decent chemistry textbook will cover this). I note however that my initial thoughts above on oxidation being a direct factor in decay appear to be wrong: what appears to happen is that specific enzymes that are normally active under controlled circumstances in living cells begin attacking the cell's own tissues in death, presumably because of the absence of the controls present in life, and reducing agents act to denature those enzymes and prevent them from attacking the cell's own integument. Nice to know I can learn something new from papers such as this. :)

When reducing agents were present in the environment containing the dead embryos, those reducing agents did indeed halt normal decay processes, and the particular chemical signs of enzyme inactivation pertinent to this were detected. Apparently the enzymes in question rely upon disulphide bonds to maintain their integrity, and reducing agents break these, thus causing the enzymes to undergo radical structural change with respect to protein folding, which destroys the active lytic sites. Disulphide bonds can be found in a number of critical proteins, such as, for example, insulin, and are usually formed post-translation by other enzymes, frequently between cysteine molecules. Break the disulphide bonds between the cysteine molecules, which are formed by oxidising enzymes (hence reducing agents will reverse the process) and the enzymes cease functioning.

So, the authors have established direct evidence that their sea urchin embryos can be preserved in a reducing environment, and have even detected the chemical basis for this preservation. Let's move on again ...

Raff et al, 2006 wrote:Role of Embryo Size.

The preponderance of reported large-sized embryos (10, 11, 30) in fossil fauna raised the possibility that large size might be a determinant in survival for mineralization. We therefore also examined preservability of the much smaller embryos of a planktotrophic sea urchin from another family, Lytechinus pictus. L. pictus eggs are only 100 μm in diameter and have a more inflated and apparently more fragile fertilization envelope than H. erythrogramma. L. pictus cleavage-stage embryos exhibited identical responses to our test conditions as the much larger H. erythrogramma embryos. Dead two- and four-cell L. pictus embryos placed in reducing conditions retained their fertilization envelopes and blastomere morphology for up to 4 weeks (Fig. 3A), whereas killed embryos returned to normal seawater underwent autolysis within a few hours postdeath (Fig. 3B). These data and taphonomy of later-stage embryos described below show that size is not a key factor in preservation.


So, by changing species to one with a much smaller embryo, the authors established that size is not an intrinsic factor in determining preservation when a suitable reducing environment is present - embryos of different sizes exhibit much the same level of preservation. Which adds weight to the notion that the fossil record in this respect is subject to an additional mechanism favouring large size.

Raff et al, 2006 wrote:Role of the Fertilization Envelope.

An unexpected factor in potential preservation of embryos is the crucial role of the fertilization envelope. Under reducing conditions both large lipid-rich embryos of a direct developer and small protein yolk-based embryos of an indirect developer could be preserved for prolonged times when the fertilization envelopes were intact. To further assess the role of the fertilization envelope we tested preservation of blastula-stage embryos from both small- and large-egged species before and after hatching. Examining embryos after release from the fertilization envelope mediated by the normal hatching process circumvented artefacts because of weakening or distortion of embryos that we have sometimes observed during mechanical or chemical removal of the fertilization envelope at earlier stages.

If killed prehatching blastulae were returned to normal seawater, the individual cells underwent autolysis, followed by degeneration of the fertilization envelopes and bacterial decay. Under reducing conditions, the preservation potential of killed prehatching blastulae was similar to cleavage-stage embryos, but retention of normal morphology was not as good as in cleavage stages. Under reducing conditions, the normal columnar shape of cells of unhatched L. pictus blastulae was lost; cells rounded up, cell–cell adhesion was diminished, and the blastocoels collapsed, producing a stereoblastula-like morphology (compare Fig. 3 C and D). Interpretation of developmental morphology in potential fossils at this stage would thus be misleading. The clusters of blastomeres in these preserved L. pictus blastulae resemble some of the rarer Doushantuo fossil embryo-like forms with hundreds of cells and poorer preservation than the more common cleavage-stage forms (1, 30). Unhatched H. erythrogramma blastulae behaved similarly. It thus appears that cell–cell adhesion is not sufficient in later-stage embryos to maintain faithful morphological architecture under reducing conditions.


So, the authors have established that later stage embryos (blastula stage) are less likely to retain their features faithfully even in a reducing environment than cleavage-stage embryos, and consequently care needs to be exercised when attempting to interpret putative embryo fossils.

Raff et al, 2006 wrote:Unhatched L. pictus blastulae exhibited similar preservational potential to cleavage stages, remaining well preserved in reducing conditions for at least 3 weeks. Unhatched H. erythrogramma blastulae showed slightly less preservational potential, caused in part by the accumulation of large lipid droplets. Some experimental samples began to degrade after 1 week.


So, a range of factors are already manifesting themselves as being implicated in the degree to which preservation of embryonic material occurs, and that the picture is a fairly complex one. Cleavage-stage embryos are apparently the best preserved, and exhibit more or less uniform preservation in reducing environments regardless of size or species. Later stage embryos with more complex tissue differentiation, on the other hand, begin to exhibit features that complicate the picture, making preservation of these stages more problematic and requiring additional specialised conditions.

Raff et al, 2006 wrote:Reducing conditions did not support preservation of any posthatching stages lacking a fertilization envelope for any of the three sea urchin species we examined (Figs. 3 E and F and 4). The morphology of newly hatched L. pictus blastulae is very similar to unhatched blastulae (Fig. 3E), and so is the behavior of the cells when placed in reducing conditions after killing the embryos. In seawater containing β-ME, cells from hatched blastulae quickly rounded up and lost the tight cell–cell adhesion of the living embryo. In the absence of the constraining fertilization envelope, the embryos rapidly fell apart (Fig. 3F). Killed hatched H. erythrogramma blastulae behaved similarly under reducing conditions. Individual cells might be preserved for extended periods in reducing conditions, but it would be difficult indeed to identify their fossilized remains.


So, the fertilisation envelope is crucial to good preservation, and consequently, early stages are more likely to be preserved under reducing conditions than later stages. Embryos that have hatched and emerged from the fertilisation envelope are least likely to be preserved well, and indeed are likely to disintegrate.

Raff et al, 2006 wrote:Although they possess differentiated cell layers and well integrated internal tissue architecture, H. erythrogramma larvae also lost morphological integrity within a day or less under reducing conditions (Fig. 4 A and B). Likewise pluteus larvae from the indirect-developing, planktotrophic sister species, Heliocidaris tuberculata (Fig. 4 C–J), were not preserved in seawater containing β-ME. Moreover, calcitic skeletal elements rapidly dissolved in the highly reducing conditions that would potentially support phosphatization processes of fossilization of soft tissues (Fig. 4E). Skeletal elements were stable in less severe reducing conditions or in normal seawater (Fig. 4 F–I), environments incompatible with preservation of cell structure.


So, for hatched embryos, the situation is even worse, because features that would normally be preserved under non-reducing conditions are degraded under the reducing conditions that are required to foster soft tissue preservation for sufficient time to ensure the initialisation of phosphatisation.

The discussion section that follows is long, and hence I shall simply highlight the important parts.

Raff et al, 2006 wrote:Discussion

Our results show that several factors may affect fossilization of embryos (Table 1). Both the correct chemical environment and the presence of a fertilization envelope are key. Even when contained within a fertilization envelope, soft-bodied embryos and larvae in normal seawater are subject to internal autolytic decay processes. Without a fertilization envelope, they are subject to both autolysis and external action by bacterial decay and action of protists. In reducing conditions compatible with mineralization, autolysis is blocked and extended preservation is possible, but only if the embryo is enclosed within the fertilization envelope. The fertilization envelope may facilitate establishment of a geochemical microenvironment that inhibits decay and allows authigenic mineralization.

These data suggest strong taphonomic biases in distribution of fossil embryos. First, fossils of cleavage-stage embryos in fertilization envelopes should reflect a broad phylogenetic spectrum. Throughout much of marine animal diversity, early developmental stages are surrounded by envelopes that harden at fertilization and surround the embryos until hatching, including embryos of many species within cnidarians, annelids, phoronids, bryozoans, nematodes, arthropods, hemichordates, echinoderms, ascidians, and vertebrates (31–34). This wide distribution among living marine clades suggests that fertilization envelopes were likely also widely distributed in Late Precambrian and Cambrian marine embryos. The presence of large numbers of fossilized embryos in early cleavage stages in the Doushantuo fauna (1, 6, 11) fits with the feasibility of preservation suggested by our data.

Second, hatched embryos and soft-bodied larvae are unlikely to be preserved even under reducing conditions. In light of these results, claims of fossilized larvae among the Doushantuo fauna (2, 3), already the subject of critical analysis (5, 14, 35), appear even more unlikely. In addition, the nonequivalence of preservational potential for different developmental stages means that there would likely be a gap in the fossil record for ontogeny of many species. Our data coupled with previous taphonomic studies (15–18) suggest we should expect to find fossils of early stages and later cuticularized developmental stages but not hatched blastulae or primary larvae. This preservation bias may produce an artifact of interpretation of fossil faunas in which common cleavage-stage embryo fossils might not relate to similar-sized fossils of preadult stages.

Our data provide clues for interpreting the morphology of fossil embryos. Rapid death maintains blastomere numbers and shape, whereas slow death produces aberrant embryos. Thus, although concern has been expressed over the patterns of cleavage exhibited by Doushantuo embryos (36, 37), the equal size of the blastomeres within these embryos suggests rapid death and a faithful representation of the living embryo. The embryos from the Lower Cambrian of Shaanxi (6, 11, 38), exhibiting unequal blastomere size, are more difficult to interpret. The irregular pattern could be explained by slow death. However, some cleavage-stage embryos, such as those of spiralians, have different-sized blastomeres; also, in stages where hundreds of cells may be present, some embryos have cells of unequal size that are less evenly spaced. Nonetheless, a general feature of early cleavage embryos is that cells have a regular and coherent arrangement, unlike the irregular cell patterns such as in Fig. 1 J and K. Moreover, embryos that have undergone abnormal fertilization, as in polyspermy (Fig. 1L), exhibit abnormal cleavages unrelated to the events that killed or preserved them.

We found that many modes of rapid death do not disrupt embryos. However, hypotonic seawater, a plausible cause of death in situ, resulted in changes to blastomere volume and shape (Fig. 1G). Doushantuo cleavage embryos show a range of morphologies in which the blastomeres are more or less tightly adpressed to one another (1) or to the fertilization envelope (39). Another possible artifact might arise from our observation that even under reducing conditions fidelity of normal architecture was not fully maintained in blastula stages. Such differences in morphology in fossil forms might represent different species or even a change in cleavage pattern during development of a single species, but also might be artefacts of taphonomic variables. Attempts to discriminate developmental series of different species in fossil deposits (11) have not considered such artefacts.

In some cases the fossils may provide clues to nonideal prefossilization conditions. For example, Xiao and Knoll (25, 30) inferred organic degradation in some of the Doushanto embryos, the appearance of which is similar to some of our experimental embryos under nonpreserving conditions (Fig. 3 B and D). Some of the poorly preserved fossils interpreted as hydrozoan gastrulae (2) also resemble these degraded embryos.

Understanding potential taphonomic biases in the preservation of Precambrian and Cambrian fossil embryos provides a window on the metazoan radiation and the origins of larvae (40). Hypotheses of developmental evolution among metazoan phyla formulated on the basis of a fossil record devoid of primary larvae (12, 35) may be spurious. Rather, the evolution of life history and developmental modes in early metazoans may have to be inferred indirectly from fossil embryos.

We observed that decay and preservation potential were similar in both the large lipid-rich direct developing H. erythrogramma embryos and small yolk-rich embryos from two species of planktotrophic indirect developers, indicating that size and cytoplasmic composition may have little influence on taphonomy of sea urchin embryos and larvae. The Doushantuo fauna reflects a developmental-stage bias consistent with taphonomic observations, but the fauna reported to date contains only larger embryos. This finding may result from a preponderance of large-egged direct developers in the fauna, a biostratinomic artifact, or an artifact of sampling microfossils of smaller sizes.

The distribution of fossil embryo sizes is significant because in modern marine fauna, large egg size (>300 μm) and lecithitrophy, and small egg size and planktotrophy, are strongly linked with direct and indirect development, respectively. We show that the primary larvae of indirect developers are unlikely to be preserved. Reinterpretation of the embryo fossil record in this light suggests that the absence of primary larvae is probably a taphonomic artifact and, as such, it may never prove possible to directly test hypotheses on the life-history strategy adopted by early metazoans. However, fossil embryos in the small size range can be used as a marker for the presence of feeding larvae. A shift associated with the Cambrian radiation from predominantly direct development to mainly planktonic feeding larvae should leave a signal of a change in size distribution in fossilized cleavage-stage embryos. Based on extant species, a size shift from 300 μm or more diameters to a smaller diameter range from 60 to 200 μm would be predicted.

There are convincing arguments that feeding larvae were present in several taxa by the early Ordovician (41, 42); thus comparisons of embryo fossils from the late Precambrian through the early Ordovician (13, 42) would allow this question to be answered. If small-sized embryos typical of planktotrophic indirect-developers are present in late Cambrian to early Ordovician sediments but absent in late Precambrian to early Cambrian deposits, this pattern would be consistent with a later appearance in evolution. In contrast, if small-sized embryos cannot be found in deposits from time periods when feeding larvae are known to exist, then their absence from other deposits is likely to be a taphonomic bias and would not be informative. Thus even though we cannot expect to find larvae themselves in the fossil record, the robust predictions supported by size classes of modern embryos will allow interpretation of life history and developmental mode of fossil fauna, once it is known if the size range of fossil embryo faunas is real or if microfossils representing small-sized embryos are present but heretofore unsampled.


So, in other words, experiments on present day sea urchin embryos indicate that it is possible to infer evolutionary conclusions about the development of specific traits in certain lineages based upon the appearance of embryos of specific sizes and their relative abundance once microfossils are subject to appropriate proper analysis. Indeed, the authors have already made a prediction above about the features that should be observed in microfossil populations, given the connection between certain developmental traits and embryo size in the respective lineages. It is also possible to determine in advance what patterns of microfossil distribution would fail to be evolutionarily informative with respect to these lineages, as stated above. Therefore, the experiments allow us to arrive at reasonable conclusions about those lineages, based upon future examination of microfossil populations in the light of these experimental results.

So, what to make of AiG's nonsense in the light of the above?

Let's take a look at their suppurating, droolingly encephalitic nonsense shall we? As usual, personal pronouns addressed to whoever wrote this steaming pile of crap.

AiG Creotard Tripe wrote:Embryos disprove evolution


Verminous and pestilential sub-amoeboid dreck of the most excremental order.

Learn once and for all that the physical sciences deal in evidential support, and that proof is restricted to mathematics.

AiG Creotard Tripe wrote:Last year in China, geologists discovered fossilized animal embryos, which evolutionists


Oh here we go again with the "evolutionist" canard.

Hello, AiG, are you paying attention? Then learn THIS lesson once and for all ...

There is no such thing as an "evolutionist". There are evolutionary biologists, namely the specialist scientific professionals who devote decades of their lives to studying and researching their field, and persons outside that specialist field who accept the evidence-based, reality-based case that said scientists present for evolutionary hypotheses. The word "evolutionist" is a discoursive elision deployed by creationists for the mendacious purpose of trying to suggest that valid evolutionary science is a "doctrine" or a "dogma", and therefore is conceptually symmetrical to their doctrine. NO such "symmetry" exists, and furthermore, since evolutionary biology provides critically robust evidential support for its hypotheses, it is not a "doctrine" or a "dogma". The absurdity and mendacity of this discoursive elision becomes manifest when one asks as a corollary, does accepting the validity of gravity make one a "gravitationalist", or accepting the validity of electromagnetism make one an "electromagnetist"?

Now either learn this lesson or fuck off back to remedial class where you belong, capiche?

AiG Creotard Tripe wrote:believe to be 600 million years old.


WRONG. AGAIN.

There is NO "belief" involved. The rock layers above and below the specimens in question were precisely dated, thus providing an effective upper and lower limit on the age of the specimens in question, using dating techniques that are robust and rigorous (please, spare me your nonsense that radiometric dating is based upon "assumptions", go and learn some basic physics). "Belief" is something that REAL SCIENTISTS leave to purveyors of worthless masturbation fantasies such as yourselves.

AiG Creotard Tripe wrote:One would logically assume that if evolution were true, modern embryos, after hundreds of millions of years of evolution, would be very different from those found in China.


TOTAL BOLLOCKS.

Someone doesn't know their basic embryology, do they?

Strange, is it not, that the early stages of embryological development are unchanged right across taxonomic phyla. It is only later in the developmental process that the phyletic differences begin to manifest themselves. During the cleavage stage, and for that matter during the earliest phases of the blastula stage, without knowing what species the parents belong to, it is, without a direct DNA test, impossible to determine what species that embryo is. Embryos from right across different taxonomic phyla, from cnidarians through arthropods, annelids, molluscs right the way through to chordates, including ALL vertebrates, exhibit IDENTICAL cell division features and only start to manifest differences later, when the appropriate signalling and regulatory genes enforce the differences by building upon the basic HOX gene bauplan according to different regulatory régimes. Now, since these different phyla ALL have identical earliest embryonic stages, this, if anything, merely reinforces the case for common descent, as of course does the possession of entire families of homologous genes such as the HOX genes, the Pax genes, the bmp, wnt and hh signalling genes ... beginning to get the picture here are you?

AiG Creotard Tripe wrote:The China embryos, however, appear to be identical to those of animals living today.


Which, given the above observed facts from developmental embryology right across taxonomic phyla, is not wholly unexpected. What part of this elementary concept are you too stupid to understand?

AiG Creotard Tripe wrote:Because evolutionist researchers are committed to their belief in a very old geologic column


BULLSHIT.

Apart from the resurrection of the "evolutionist" canard for the second time, we see again the erection of the specious "belief" canard, when there is NO "belief" involved, as stated above. The hard evidence from the real world supports an ancient geological history for the planet, which means that reality sticks the middle finger to your worthless mythology-based nonsense. Hard evidence such as radiometric dating, which, despite the bleating and whining of reality-denial masturbation fantasists everywhere, is NOT based upon "assumptions", but upon a well-understood and long-studied physical process that is governed by a precise mathematical law, a precise mathematical law that was derived from direct empirical observation of radionuclide decay in the laboratory. So don't try and palm this bullshit off on us either.

AiG Creotard Tripe wrote:they automatically assume the embryos found in China are hundreds of millions of years old.


BULLSHIT.

The scientists "ASSUMED" PRECISELY NOTHING. They dated the rock strata above and below the fossils and arrived at a set of upper and lower limit bracketing dates for the fossils as a direct experimental result. Once again, what part of "directly measuring the age of the rocks using a well-understood and rigorous technique based upon a well-understood physical process, that in turn is governed by a precise mathematical law, does NOT equal 'assuming' the age in any logically consistent universe" are you either too stupid or too duplicitous to understand? Oh, but then this is AiG we're talking about here ... you're both.

AiG Creotard Tripe wrote:The most logical and defendable explanation, however, is that these fossils were formed quickly and catastrophically, most likely during the Flood of Noah’s time 4,300 years ago.


TOTAL BOLLOCKS.

This is festeringly putrid, suppurating, bubotic wankery of the most fulminating order, a notion that is so palsied and scientifically illiterate that if it were written on paper, it would be unfit to use as toilet paper for incontinent baboons.

Let me spell this out to you in words even a creationist can understand.

YOUR FANTASY FLOOD NEVER HAPPENED. OBSERVATIONAL REALITY SAYS IT NEVER HAPPENED. My tropical fish, which are happily alive and frolicking in their aquaria, are laughing at you, because they would never have existed if your fantasy flood had taken place. ALL of the Ostariophysan fishes would now be EXTERMINATED. None of them would be left. The fact that they are, and that several of them have been spawning rampantly in my aquaria over the past five years, producing three generations of offspring, sticks the middle finger to your witless, foetid, utterly diseased masturbation fantasy about the ridiculous flood and the 600 year old drunken barge captain you jerk off to.

*** ORIGINAL POST ENDS ***

Now, when I originally wrote the above post, dated 17th September 2008, I was of the view that oxidation was the means by which decay began. Whilst oxidation does play a role in some decay processes, the processes that result in tissue disintegration frequently fall into a class of processes called 'autolytic', a word which derives from Classical Greek, roughly translating as "self-breaking". This is because living cells contain proteolytic enzymes, which exist in order to allow those cells to break down certain proteins, and use the products of said breakdown for the formation of new proteins. In life, this happens in a controlled manner, with various, other regulatory enzymes directing those proteolytic enzymes toward the proper targets. After death, however, those regulatory enzymes cease to function, and the proteolytic enzymes start breaking down proteins indiscriminately, including the proteins comprising the superstructure of the now-dead cells.

Now, it would make sense, from the standpoint of plant reproduction, for fruits to contain proteolytic enzymes accelerating the decomposition process in the case of fallen fruits, because the object of the exercise is to disperse the plant's seeds into a nutrient rich environment with as much speed and efficiency as possible. It would therefore make sense for fruit flesh to contain an abundance of proteolytic enzymes of this sort. Indeed, one of the tricks I use in cooking, when firing up a steak casserole, is to use pineapple juice as a tenderiser for the steak - pineapple juice is particularly rich in proteolytic enzymes, and when you marinate a steak in pineapple juice, you can tenderise even the toughest of cuts so that it becomes suitably tender and tasty on the end of your fork after cooking. Additional support for this comes from the experience of some escaping Far Eastern prisoners of war, who, after escaping from captivity at the hands of the Imperial Japanese Army during World War II, alighted upon a field in which pineapples were growing, and ate nothing but pineapples for an extended period of time. The proteolytic enzyme in pineapples, known as bromelain, attacked the gum tissues of the escaping prisoners in question, to the point where their teeth fell out.

However, as always, it's advisable to go and hunt for some scientific papers. One apposite paper is this one:

Tomato Fruit Cell Wall. I. Use Of Purified Tomato Polygalacturonase And Pectinmethylesterase To Identify Developmental Changes In Pectins by James L. Koch and Donald J. .Nevins, Plant Phsyiology, 91: 816-822 (1st June 1989) [Full paper downloadable from here]

Koch & Nevins, 1989 wrote:ABSTRACT

Cell wall isolation procedures were evaluated to determine their effect on the total pectin content and the degree of methylesterification of tomato (Lycopersicon esculentum L.) fruit cell walls. Water homogenates liberate substantial amounts of buffer soluble uronic acid, 5.2 milligrams uronic acid/100 milligrams wall. Solubilization appears to be a consequence of autohydrolysis mediated by polygalacturonase II, isoenzymes A and B, since the uronic acid release from the wall residue can be suppressed by homogenization in the presence of 50% ethanol followed by heating. The extent of methylesterification in heatinactivated cell walls, 94 mole %, was significantly greater than with water homogenates, 56 mole %. The results suggest that autohydrolysis, mediated by cell wall-associated enzymes, accounts for the solubilization of tomato fruit pectin in vitro. Endogenous enzymes also account for a decrease in the methylesterification during the cell wall preparation. The heat-inacffvated cell wall preparation was superior to the other methods studied since it reduces [chr]946]-elimination during heating and inactivates constitutive enzymes that may modify pectin structure. This heat-inactivated cell wall preparation was used in subsequent enzymatic analysis of the pectin structure. Purified tomato fruit polygalacturonase and partially purified pectinmethylesterase were used to assess changes in constitutive substrates during tomato fruit ripening. Polygalacturonase treatment of heat-inactivated cell walls from mature green and breaker stages released 14% of the uronic acid. The extent of the release of polyuronides by polygalacturonase was fruit development stage dependent. At the tuming stage, 21% of the pectin fraction was released, a value which increased to a maximum of 28% of the uronides at the red ripe stage. Pretreatment of the walls with purified tomato pectinesterase rendered walls from all ripening stages equally susceptible to polygalacturonase. Quantitatively, the release of uronides by polygalacturonase from all pectinesterase treated cell walls was equivalent to polygalacturonase treatment of walls at the ripe stage. Uronide polymers released by polygalacturonase contain galacturonic acid, rhamnose, galactose, arabinose, xylose, and glucose. As a function of development, an increase in the release of galacturonic acid and rhamnose was observed (40 and 6% of these polymers at the mature green stage to 54 and 15% at the red ripe stage, respectively). The amount of galactose and arabinose released by exogenous polygalacturonase decreased during development (41 and 11% from walls of mature green fruit to 11 and 6% at the red ripe stage, respectively). Minor amounts of glucose and xylose released from the wall by exogenous polygalacturonase (4-7%) remained constant throughout fruit development.


Another paper that points to the existence of proteolytic enzymes or proteases in fruit is this one:

Cucumisin, A Serine Protease From Melon Fruits, Shares Structural Homology With Subtilisin And Is Generated From A Large Precursor by Hiroshi Yamagashi, Takuya Masuzawa, Yuko Nagaoka, Tatsuji Ohnishi and Teruo Iwasaki, The Journal Of PLant Biochemistry, 298(52): 32725-32731 (30th December 1994) [Full paper downloadable from here]

Yamagashi et al, 1994 wrote:Cucumisin is a thermostable alkaline serine protease that is found in the juice of melon fruits (Cucumis melo L.). We have determined the complete nucleotide sequence of a cucumisin cDNA (2,552 nucleotides) and deduced the corresponding amino acid sequence. The open reading frame of the cDNA consists of 731 codons and encodes a large precursor (molecular weight, 78,815) relative to the observed size of mature native cucumisin (67 ma). Sequence comparisons reveal that cucumisin has several features in common with the microbial proteases of the subtilisin family. The highly conserved sequences to the proximal regions of the catalytic triad amino acids Asp, His, and Ser, together with the substrate binding site in subtilisin, can be found within the deduced amino acid sequence of the protease domain of the cucumisin precursor. Cucumisin is the first known plant protease with such characteristics. Examination of the primary structure of cucumisin revealed that it is synthesized as a precursor, consisting of four functional domains: a possible signal peptide (22 amino acid residues), an NH,-terminal pro-sequence (88 residues), a 54-kDa protease domain (505 residues), which is the active enzyme domain of the 67-kDa native cucumisin, and a 14-kDa COOH-terminal polypeptide (116 residues), which arises by limited autolysis of the 67-kDa native cucumisin. This structure of cucumisin suggests that it is probably synthesized as an inactive precursor.


Another apposite paper is this:

Cell Wall Autolysis During Kiwifruit Development by P. P. Gallego & I. Zarra, Annals of Botany, 81: 91-96 (1998) [Full paper downloadable from here]

Gallego & Zarra, 1998 wrote:Cell walls prepared from developing kiwifruits showed autolytic activity. The proteins extracted from active walls were also able to release carbohydrates from inactive cell walls. Analysis of the sugars released, using both procedures, showed that uronic acids were the major component, especially during the first hours of incubation, although neutral sugars such as glucose and galactose were also present. Most of the carbohydrates autolytically released from the cell wall eluted in the void volume on a Bio Gel P2 column. However, carbohydrates released from inactive cell walls by the protein extract mostly eluted in the monosaccharide uronic acid and glucose peaks. The autolytic activity of isolated cell walls, as well as the glycosylhydrolase activity of the proteins extracted from the cell walls, showed important changes during fruit development. The diåerences between autolytic activity and the glycosylhydrolase activity against the cell wall suggest that the glycosylhydrolases `in muro' are subjected to some regulatory mechanism which disappears with their extraction. Finally, the role of glycosylhydrolases, such as polygalacturonases and galactosidases, in relation to cell wall changes in fruits, is discussed.


Basically, there's a vast literature on autolysis in fruit, and a number of important proteolytic enzymes are documented. :)
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Re: Why do fruits rot?

#18  Postby quas » Feb 16, 2012 4:03 am

Callilasea, are the reactions of the enzymes sped up by the ripening process?

Callilasea wrote:Now, it would make sense, from the standpoint of plant reproduction, for fruits to contain proteolytic enzymes accelerating the decomposition process in the case of fallen fruits, because the object of the exercise is to disperse the plant's seeds into a nutrient rich environment with as much speed and efficiency as possible. It would therefore make sense for fruit flesh to contain an abundance of proteolytic enzymes of this sort. Indeed, one of the tricks I use in cooking, when firing up a steak casserole, is to use pineapple juice as a tenderiser for the steak - pineapple juice is particularly rich in proteolytic enzymes, and when you marinate a steak in pineapple juice, you can tenderise even the toughest of cuts so that it becomes suitably tender and tasty on the end of your fork after cooking. Additional support for this comes from the experience of some escaping Far Eastern prisoners of war, who, after escaping from captivity at the hands of the Imperial Japanese Army during World War II, alighted upon a field in which pineapples were growing, and ate nothing but pineapples for an extended period of time. The proteolytic enzyme in pineapples, known as bromelain, attacked the gum tissues of the escaping prisoners in question, to the point where their teeth fell out.

Is it the pineapple enzymes or the acid responsible for the denaturing of proteins in steaks and gum tissues?
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Re: Why do fruits rot?

 
 

Re: Why do fruits rot?

#19  Postby Calilasseia » Feb 16, 2012 5:02 am

It's the proteolytic enzyme, bromelain, that does the work. Don't forget that most of the acids present in fruits are carboxylic acids that participate in the Krebs cycle, an essential cycling of nutrients that takes place in vast swathes of the biosphere, which are themselves the subject of enyzmatic activity in that cycle.
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