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Author Topic:   Potential falsifications of the theory of evolution
Taq
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Posts: 10085
Joined: 03-06-2009
Member Rating: 5.6


Message 736 of 968 (603235)
02-03-2011 1:23 PM
Reply to: Message 735 by molbiogirl
02-03-2011 12:51 PM


Re: TEs random with respect to fitness
Just to re-emphasize your point. . .
Something also struck me as interesting. Shapiro likes to draw analogies between these genetic engineering systems and what molecular biologists do in the lab. He suggests that cells use some of the same techniques that we do when restructuring their genome.
As it turns out, molecular biologists do use transposons to create mutant strains. They usually call it random transposon mutagenesis. The whole point of a transposon mutagenesis is to create a library of cells with genes that are randomly knocked out. The choice of transposons is often based on the random nature of their insertion with respect to which genes are being knocked out. If transposons only inserted into specific genes in response to specific stimuli they would be useless in the lab for the purposes of library construction.
I have constructed my own transposon libraries. After testing 1700 individual clones for specific enzyme production I finally found the knockout, and that was after dual screening for drug resistance to make sure the transposon was even inserted into the genome. I would have been uberpissed if that transposon was overly biased so that it never inserted into the gene of interest. I was pissed enough that it took 1700 clones to find the one I was looking for.

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Percy
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Posts: 22505
From: New Hampshire
Joined: 12-23-2000
Member Rating: 5.4


Message 737 of 968 (603269)
02-03-2011 2:50 PM
Reply to: Message 732 by shadow71
02-03-2011 12:07 PM


Re: Cite
Hi Shadow,
You received the answers we pretty much expected you would. We were pretty sure his responses would use the term non-random in the same misleading way as in his other writings. One good question we should have thought of was, "Do cells produce mutations they know will be advantageous?" because that's what you think Shapiro is really saying.
Nevertheless, congratulations on composing an email that drew a response. Well done!
--Percy

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Replies to this message:
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RAZD
Member (Idle past 1435 days)
Posts: 20714
From: the other end of the sidewalk
Joined: 03-14-2004


Message 738 of 968 (603444)
02-04-2011 1:19 PM
Reply to: Message 737 by Percy
02-03-2011 2:50 PM


Re: Cite
Hi Percy
You received the answers we pretty much expected you would. We were pretty sure his responses would use the term non-random in the same misleading way as in his other writings.
His response was pretty much bang-on for what I expected from the questions. I disagree somewhat with your comment re non-random - as he does clarify that by saying rather emphatically that it is not deterministic, which is shadow71's interpretation.
If it were non-random then his comment re purifying selection would not be necessary -- there would be no need to weed out deleterious mutations, and "purify" the population to have beneficial and neutral mutations.
Enjoy.

we are limited in our ability to understand
by our ability to understand
Rebel American Zen Deist
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This message is a reply to:
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RAZD
Member (Idle past 1435 days)
Posts: 20714
From: the other end of the sidewalk
Joined: 03-14-2004


Message 739 of 968 (603460)
02-04-2011 2:27 PM
Reply to: Message 734 by Taq
02-03-2011 12:34 PM


Re: Cite
Hi Taq,
He considers increasing the random mutation rate in times of stress to be a sentient reaction. Interesting, but I personally wouldn't call it sentient.
He is stretching the point, imho, however he also qualifies it:
quote:
I prefer terms like cognitive or sentient, meaning based up the acquisition and utilization of information.
Meaning that it is a learned response, learned by trial and error. The learned response is to open the gates to increased mutation, as such acquired information from past generations does not necessarily work for new ecological challenges -- except the increase in mutation rate.
He also makes what I consider false or poor statements:
quote:
The neo-Darwinian Modern Synthesis could not account for the evolution of antibiotic resistance in the latter 20th Century. It also does not explain much in the genome sequence record.
This is more assertion than fact. I see no problem with mutation and selection accounting for the evolution of antibiotic resistance across the board. Once such mutation has occurred in a bacteria then it can pass it on by HGL, but the mutation and selection are still at work in cases without HGL.
Darwin knew nothing of horizontal transfer, whole genome doublings or natural genetic engineering capabilities and neglected symbiosis. His ideas were based strictly on vertical inheritance, and he insisted on gradualism.
Darwin new nothing about genetics, apparently not even aware of Mendel's work. He did however know that traits were inherited and that this allowed natural selection to work on populations.
Darwin did not "insist" on gradualism, in fact he discussed changes in rates of evolution as entirely possible. He was just of the opinion that gradualism was more likely.
Enjoy.

we are limited in our ability to understand
by our ability to understand
Rebel American Zen Deist
... to learn ... to think ... to live ... to laugh ...
to share.


Join the effort to solve medical problems, AIDS/HIV, Cancer and more with Team EvC! (click)

This message is a reply to:
 Message 734 by Taq, posted 02-03-2011 12:34 PM Taq has replied

Replies to this message:
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Taq
Member
Posts: 10085
Joined: 03-06-2009
Member Rating: 5.6


Message 740 of 968 (603478)
02-04-2011 3:09 PM
Reply to: Message 739 by RAZD
02-04-2011 2:27 PM


Re: Cite
This is more assertion than fact. I see no problem with mutation and selection accounting for the evolution of antibiotic resistance across the board. Once such mutation has occurred in a bacteria then it can pass it on by HGL, but the mutation and selection are still at work in cases without HGL.
I think it is fair for Shapiro to note that HGT was a driving force in the latter 20th century for antibiotic resistance compared to independent acquisition through lineage specific mutations.
What is interesting to note is that HGT is still random in a way. When plasmids are passed along or picked up from the environment the bug has no way of knowing if that DNA will help them.
Darwin new nothing about genetics, apparently not even aware of Mendel's work. He did however know that traits were inherited and that this allowed natural selection to work on populations.
Darwin did not "insist" on gradualism, in fact he discussed changes in rates of evolution as entirely possible. He was just of the opinion that gradualism was more likely.
This goes back to one of my earlier criticisms. Shapiro often equivocates Darwinian evolution and Neo-Darwinian evolution. He starts out criticizing Neo-Darwinism and then talks about Darwin being ignorant of genetics. This ignores that fact that HGT, punctuated equilibria, environmentally adjustable mutation rates, transposon mutagenesis, and all of the other mechanisms he talks about were already part of the Neo-Darwinian synthesis. He makes a strawman argument of sorts.

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Taq
Member
Posts: 10085
Joined: 03-06-2009
Member Rating: 5.6


Message 741 of 968 (603480)
02-04-2011 3:14 PM
Reply to: Message 738 by RAZD
02-04-2011 1:19 PM


Re: Cite
he does clarify that by saying rather emphatically that it is not deterministic, which is shadow71's interpretation.
Shapiro claims that non-random and strictly deterministic are not synonymous. It is the qualifier (strictly) that bothers me. It borders on the "a little bit pregnant" argument. Either something is determinstic or it isn't. So I guess we can conclude that these genetic engineer systems produce mutations that are kind of non-random in a non-deterministic fashion that is blind to fitness. IOW, they are random with respect to fitness.

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shadow71
Member (Idle past 2964 days)
Posts: 706
From: Joliet, il, USA
Joined: 08-31-2010


Message 742 of 968 (603487)
02-04-2011 3:37 PM
Reply to: Message 737 by Percy
02-03-2011 2:50 PM


Re: Cite
Hi Percy. I was quite pleased that Dr. Shapiro was so accommodating. He obviously cannot defend his answers on this page and I am not qualifed to do so. For the most part I have read the comments so far and I have a few questions.
Dr. Shapiro wrote;
Has NATURAL GENETIC ENGINEERING changed the modern Darwinian theory of evolution as we know it today?
Of course. Going from random accidents to regulated biochemical systems as the source of genetic variation is a fundamental change. It allows us to understand how outside events can trigger change (see table in my 2006 "Genome Informatics" article), makes it clear how combinatorial change can occur using established adaptive components (e.g. protein domains, regulatory modules), and provides a way to investigate what kind of heuristic guidance may be operating in genome change.
Do you all disagree with his assertion that Natural Genetic Engineering has changed the modern Darwinian theory? Not necessarily falisfied it, but changed it?
To me it does appear that he is correct in stating that there is regulation in the cell and genome as initially discovered by Barbara McClilntock, and affirmed by many others.
I am still trying to understand what is meant by random mutation. Although it may not be determistic, it seems that the alternatives to random mutation may be so limited that it is really not random, but allows such a small choice that it may not be as imortant as stated by the modern theory.
That cell sentience may be more important than random mutation.
I am studying Dr. Shapiro's answers and the replies on this board and will have more comments in the future.

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Replies to this message:
 Message 743 by Taq, posted 02-04-2011 4:07 PM shadow71 has seen this message but not replied
 Message 744 by molbiogirl, posted 02-04-2011 4:32 PM shadow71 has replied

Taq
Member
Posts: 10085
Joined: 03-06-2009
Member Rating: 5.6


Message 743 of 968 (603496)
02-04-2011 4:07 PM
Reply to: Message 742 by shadow71
02-04-2011 3:37 PM


Re: Cite
Do you all disagree with his assertion that Natural Genetic Engineering has changed the modern Darwinian theory? Not necessarily falisfied it, but changed it?
I would argue that it had already changed due to these discoveries before Shapiro wrote the article. The Modern Synthesis has always been in flux just like all scientific theories.
One of the things that would require a rewrite of the theory is if mutations were deterministic (using Shapiro's vocabulary). That is not the case as even Shapiro agrees. Shapiro also indicates that these genetic engineering systems create a lot of variability that is then purified through selection. This fits right in with the foundation of the Modern Synthesis.
I am still trying to understand what is meant by random mutation. Although it may not be determistic, it seems that the alternatives to random mutation may be so limited that it is really not random, but allows such a small choice that it may not be as imortant as stated by the modern theory.
From my reading this isn't the case. In the case of HIV they insert into active transcription units about 80% but ASLV seems to have a very slight predilection towards transcription units:
quote:
For HIV the frequency of integration in transcription units ranged from 75% to 80%, while the frequency for MLV was 61% and for ASLV was 57%. For comparison, about 45% of the human genome is composed of transcription units (using the Acembly gene definition).
Retroviral DNA Integration: ASLV, HIV, and MLV Show Distinct Target Site Preferences - PMC
Transposons derived from the retroviruses may very well carry these dispositions as well. Shapiro would describe these insertions as non-random due to the preference for transcriptional units. However, these preferred areas still make up half of the genome, or about 1.5 billion bases, not to mention the other 1.5 billion bases that these retroviruses still insert into but at a lower frequency.
That cell sentience may be more important than random mutation.
It is the cell sentience that results in the random mutations so I don't see how you can call one more important than the other as it relates to evolution.
Edited by Taq, : No reason given.

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molbiogirl
Member (Idle past 2671 days)
Posts: 1909
From: MO
Joined: 06-06-2007


(1)
Message 744 of 968 (603498)
02-04-2011 4:32 PM
Reply to: Message 742 by shadow71
02-04-2011 3:37 PM


Defining random mutation again
I am still trying to understand what is meant by random mutation.
Let me give this another shot.
If some outside influence (stress, a chemical, UV, etc.) initiates an SOS response in an E. coli (note: an SOS response is one of the many biochemical systems Shapiro considers NGE) it amps up the mutation rate.
What mutations occur (e.g. if base substitutions, which base A/C/T/G will change) is RANDOM.
Where the mutations occur in the genome is RANDOM.
Thus, the mutations are RANDOM with respect to fitness.
The SOS response is the same every time. But it produces different results.
The SOS response can produce beneficial, neutral or deleterious mutations. It's random. There's no pre-determined endpoint.
That cell sentience may be more important than random mutation.
The SOS response is not a decision the E. coli "makes", btw. Anymore than you "decide" to increase hydrochloric acid production after you eat. It's just a biochemical response.
Edited by molbiogirl, : No reason given.

This message is a reply to:
 Message 742 by shadow71, posted 02-04-2011 3:37 PM shadow71 has replied

Replies to this message:
 Message 745 by shadow71, posted 02-04-2011 5:18 PM molbiogirl has replied

shadow71
Member (Idle past 2964 days)
Posts: 706
From: Joliet, il, USA
Joined: 08-31-2010


Message 745 of 968 (603508)
02-04-2011 5:18 PM
Reply to: Message 744 by molbiogirl
02-04-2011 4:32 PM


Re: Defining random mutation again
miobiogirl posts;
If some outside influence (stress, a chemical, UV, etc.) initiates an SOS response in an E. coli (note: an SOS response is one of the many biochemical systems Shapiro considers NGE) it amps up the mutation rate.
What mutations occur (e.g. if base substitutions, which base A/C/T/G will change) is RANDOM.
Where the mutations occur in the genome is RANDOM.
Thus, the mutations are RANDOM with respect to fitness.
The SOS response is the same every time. But it produces different results.
The SOS response can produce beneficial, neutral or deleterious mutations. It's random. There's no pre-determined endpoint
I guess this is where I am getting confused. This paper talks of Non-Random Distribution of TEs, where the TEs non-randomly occur in what appears to be selected sites.
If the mutations occur in a non-random manner, are they random with respect to fitness?
Exceptional Diversity, Non-Random Distribution, and Rapid Evolution of Retroelements in the B73 Maize Genome
Although TEs are a major component of all studied plant genomes, and are the most significant contributors to genome structure and evolution in almost all eukaryotes that have been investigated, their properties and reasons for existence are not well understood in any eukaryotic genome. In order to begin a comprehensive study of TE contributions to the structure, function, and evolution of both genes and genomes, we first identified all of the TEs in maize and then investigated whether there were non-random patterns in their dispersal. We used homology and TE structure criteria in an effort to discover all of the retroelements in the recently sequenced genome from maize inbred B73. We found that the retroelements are incredibly diverse in maize, with many hundreds of families that show different insertion and/or retention specificities across the maize chromosomes. Most of these element families are present in low copy numbers and had been missed by previous searches that relied on a high-copy-number criterion. Different element families exhibited very different biases for accumulation across the chromosomes, indicating that they can detect and utilize many different chromatin environments.
Article Metrics Related Content Comments: 1 To add a note, highlight some text. Hide notes
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Abstract
Author Summary
Introduction
Results
Discussion
Materials and Methods
Supporting Information
Author Contributions
References
Regina S. Baucom1#, James C. Estill2#, Cristian Chaparro3, Naadira Upshaw1, Ansuya Jogi1, Jean-Marc Deragon3, Richard P. Westerman4, Phillip J. SanMiguel4, Jeffrey L. Bennetzen1*
1 Department of Genetics, University of Georgia, Athens, Georgia, United States of America, 2 Department of Plant Biology, University of Georgia, Athens, Georgia, United States of America, 3 Universit de Perpignan, Via Domitia, CNRS UMR5096 LGDP, Perpignan, France, 4 Department of Horticulture and Landscape Architecture, Purdue University, West Lafayette, Indiana, United States of America
Abstract Top
Recent comprehensive sequence analysis of the 1maize genome now permits detailed discovery and description of all transposable elements (TEs) in this complex nuclear environment. Reiteratively optimized structural and homology criteria were used in the computer-assisted search for retroelements, TEs that transpose by reverse transcription of an RNA intermediate, with the final results verified by manual inspection. Retroelements were found to occupy the majority (>75%) of the nuclear genome in maize inbred B73. Unprecedented genetic diversity was discovered in the long terminal repeat (LTR) retrotransposon class of retroelements, with >400 families (>350 newly discovered) contributing >31,000 intact elements. The two other classes of retroelements, SINEs (four families) and LINEs (at least 30 families), were observed to contribute 1,991 and ~35,000 copies, respectively, or a combined ~1% of the B73 nuclear genome. With regard to fully intact elements, median copy numbers for all retroelement families in maize was 2 because >250 LTR retrotransposon families contained only one or two intact members that could be detected in the B73 draft sequence. The majority, perhaps all, of the investigated retroelement families exhibited non-random dispersal across the maize genome, with LINEs, SINEs, and many low-copy-number LTR retrotransposons exhibiting a bias for accumulation in gene-rich regions. In contrast, most (but not all) medium- and high-copy-number LTR retrotransposons were found to preferentially accumulate in gene-poor regions like pericentromeric heterochromatin, while a few high-copy-number families exhibited the opposite bias. Regions of the genome with the highest LTR retrotransposon density contained the lowest LTR retrotransposon diversity. These results indicate that the maize genome provides a great number of different niches for the survival and procreation of a great variety of retroelements that have evolved to differentially occupy and exploit this genomic diversity.
Author Summary Top
Although TEs are a major component of all studied plant genomes, and are the most significant contributors to genome structure and evolution in almost all eukaryotes that have been investigated, their properties and reasons for existence are not well understood in any eukaryotic genome. In order to begin a comprehensive study of TE contributions to the structure, function, and evolution of both genes and genomes, we first identified all of the TEs in maize and then investigated whether there were non-random patterns in their dispersal. We used homology and TE structure criteria in an effort to discover all of the retroelements in the recently sequenced genome from maize inbred B73. We found that the retroelements are incredibly diverse in maize, with many hundreds of families that show different insertion and/or retention specificities across the maize chromosomes. Most of these element families are present in low copy numbers and had been missed by previous searches that relied on a high-copy-number criterion. Different element families exhibited very different biases for accumulation across the chromosomes, indicating that they can detect and utilize many different chromatin environments.
Citation: Baucom RS, Estill JC, Chaparro C, Upshaw N, Jogi A, et al. (2009) Exceptional Diversity, Non-Random Distribution, and Rapid Evolution of Retroelements in the B73 Maize Genome. PLoS Genet 5(11): e1000732. doi:10.1371/journal.pgen.1000732

This message is a reply to:
 Message 744 by molbiogirl, posted 02-04-2011 4:32 PM molbiogirl has replied

Replies to this message:
 Message 746 by molbiogirl, posted 02-04-2011 6:12 PM shadow71 has replied
 Message 770 by Taq, posted 02-07-2011 11:41 AM shadow71 has replied

molbiogirl
Member (Idle past 2671 days)
Posts: 1909
From: MO
Joined: 06-06-2007


Message 746 of 968 (603518)
02-04-2011 6:12 PM
Reply to: Message 745 by shadow71
02-04-2011 5:18 PM


Defining random mutation and TEs again
This paper talks of Non-Random Distribution of TEs, where the TEs non-randomly occur in what appears to be selected sites.
First, Taq answered this question earlier in the thread. I suggest you re-read Messages 733, 736 & 743.
Second, please re-read my post Message 735.
Third, here is the paper you cited.
Fourth, from that paper:
However, as mentioned above and observed previously (reviewed in [44]), LINEs, SINEs and some LTR retrotransposon families accumulate preferentially in areas that are near genes.
A nonrandom distribution, shadow. Near genes.
The paper doesn't say near WHICH genes.
Overall, LTR retrotransposons are found to be most abundant in pericentromeric heterochromatin and least abundant in the more gene-rich arms on all chromosomes.
The TEs are all over the place. They hop all over the genome with MOST of them ending up in the pericentromeric heterochromatin.
The TEs do tend to hop into introns or exons but WHICH ONES? It's random!
And the paper doesn't say if the TEs are beneficial, deleterious or neutral.
Which means that the TEs are random with respect to fitness!

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Replies to this message:
 Message 747 by shadow71, posted 02-05-2011 9:03 PM molbiogirl has replied

shadow71
Member (Idle past 2964 days)
Posts: 706
From: Joliet, il, USA
Joined: 08-31-2010


Message 747 of 968 (603609)
02-05-2011 9:03 PM
Reply to: Message 746 by molbiogirl
02-04-2011 6:12 PM


Re: Defining random mutation and TEs again
molbioigirl posts
), LINEs, SINEs and some LTR retrotransposon families accumulate preferentially in areas that are near genes.
Molbiogirl writes;
A nonrandom distribution, shadow. Near genes.
The paper doesn't say near WHICH genes.
The dictionary states;
preference noun \ˈpre-fərn(t)s, ˈpre-f(ə-)rən(t)s\
Definition of PREFERENCE
1a : the act of preferring : the state of being preferred b : the power or opportunity of choosing
2: one that is preferred
The paper I cited and molbiogirl quoted from states;
Viewed from the standpoint of the TE, much of the diversity in TE populations and their arrangement takes on a new and informative light. A previous model proposed that low-copy-number TEs must insert near or into genes so that they have a reasonable chance of expression and activity in subsequent generations, while highly repetitive TEs need to avoid insertions that disrupt genes in most cases because 1000 or 10,000 such insertions would lead to a dead host [44]. Hence, abundant TEs rely on their abundance per se to guarantee transmission and the opportunity for activity in future generations. The data for LTR retrotransposon abundance versus copy number shown here agrees with this model, as does the fact that (to date) none of the high-copy-number LTR retrotransposons have been shown to cause a de novo mutation, while low-copy-number LTR retrotransposons (e.g., Bs1, Tnt1, Tos17) that make up a relatively small part of their genomes have caused many new mutations [47]—[49],[53]. The analysis of the maize genome suggests that the copy number for this transition is fairly low, 10—100 intact copies per genome (Figure 4), for this change in lifestyle. LTR retrotransposon families with copy numbers less than ten were usually found to preferentially accumulate in genic regions, while most LTR retrotransposon families with copy numbers higher than 100 were found to be enriched in gene-poor regions like pericentromeric heterochromatin.
The insertion preferences of LTR retrotransposons can contribute to their potential for more than just transcriptional activity. Elements that land in recombination-rich regions have a greater chance of inter-element unequal events that can create novel LTR retrotransposons with possible new properties [38]. Insertion into an LTR provides the opportunity to acquire the gene regulatory properties of the target LTR retrotransposon. Moreover, insertion of an LTR retrotransposon into an LTR retrotransposon would usually eliminate the target element as a potential competitor for future amplification.
Preferentially does not seem randdom to me. The TEs are in some way prefering to locate in preferred areas.
The paper concludes that the TEs have insertion preferences that
are beneficial to the TEs and by inference the cell.
I think Shapiro's view point of sentience in the cells is leading to a divergence from random to non-random.
Edited by shadow71, : No reason given.

This message is a reply to:
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Replies to this message:
 Message 748 by Dr Adequate, posted 02-05-2011 11:46 PM shadow71 has replied
 Message 749 by Percy, posted 02-06-2011 7:54 AM shadow71 has replied
 Message 750 by molbiogirl, posted 02-06-2011 11:37 AM shadow71 has seen this message but not replied

Dr Adequate
Member (Idle past 314 days)
Posts: 16113
Joined: 07-20-2006


Message 748 of 968 (603612)
02-05-2011 11:46 PM
Reply to: Message 747 by shadow71
02-05-2011 9:03 PM


Enough with the semantic games. You're surely not so dumb that you don't know what molbiogirl means by "preferentially", and there's no point in pretending that you don't understand her because she is after all contributing to this thread and can tell you. You won't get very far twisting the words of people who are actually talking to you --- it just makes you look like one more dishonest creationist, but without achieving the usual aim of creationist dishonesty, namely to deceive the biologically illiterate.

This message is a reply to:
 Message 747 by shadow71, posted 02-05-2011 9:03 PM shadow71 has replied

Replies to this message:
 Message 751 by shadow71, posted 02-06-2011 1:56 PM Dr Adequate has replied

Percy
Member
Posts: 22505
From: New Hampshire
Joined: 12-23-2000
Member Rating: 5.4


Message 749 of 968 (603625)
02-06-2011 7:54 AM
Reply to: Message 747 by shadow71
02-05-2011 9:03 PM


Re: Defining random mutation and TEs again
shadow71 writes:
Shapiro writes:
LINEs, SINEs and some LTR retrotransposon families accumulate preferentially in areas that are near genes.
Molbiogirl writes;
A nonrandom distribution, shadow. Near genes.
The paper doesn't say near WHICH genes.
Preferentially does not seem randdom to me. The TEs are in some way prefering to locate in preferred areas.
I'm not sure I see the problem. You quote Shapiro using the word "preferentially", and Molbiogirl says that that means a non-random distribution with respect to location, and then you say that "preferentially does not seem random to me," as if she had said that preferentially meant completely random.
I'm beginning to wonder if there isn't some math comprehension issue here. You've been provided explanations of what is random and non-random about things like the lottery and dice rolls, to no avail, and what Molbiogirl just said seems pretty clear, yet you interpreted it backward.
What is preferential about those genes in your quote is their insertion location, which doesn't mean non-random. Preferential in this case means statistically more likely to end up in one location than another. It would be like if Pittsburgh were playing Detroit in the Superbowl instead of the Packers. The odds would prefer Pittsburgh, but since it wouldn't be a certainty that Pittsburgh would win you couldn't call it deterministic or completely non-random. It's statistical, stochastic.
Regarding the Shapiro excerpt, what is not preferential and therefore random is the effect on fitness.
--Percy

This message is a reply to:
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Replies to this message:
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molbiogirl
Member (Idle past 2671 days)
Posts: 1909
From: MO
Joined: 06-06-2007


(1)
Message 750 of 968 (603634)
02-06-2011 11:37 AM
Reply to: Message 747 by shadow71
02-05-2011 9:03 PM


Re: Defining random mutation and TEs again
You seem to have missed the point.
From the paper:
Of the 1991 SINEs discovered, 1174 were found in the introns or UTRs (untranslated regions) of genes and 21 in putative coding exons (data not shown).
An intron is an area between exons which does not code for the protein. An exon codes for the protein.
A SINE has a 1% chance of landing in an exon.
Which exon, shadow?
Which protein will be affected?
Will that effect be helpful, harmful or neutral?
No answer?
That's because you don't know.
TEs are not deterministic.
The TEs' location in the genome is random with respect to which gene they hop next to.
The TEs' insertion in the genome is random with respect to fitness because the effect on the protein (beneficial/deleterious/neutral) is unknown.

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