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	<title>Comments on: The junk DNA myth (or lack thereof), explained one more time.</title>
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	<link>http://www.genomicron.evolverzone.com/2009/12/the-junk-dna-myth-or-lack-thereof-explained-one-more-time/</link>
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		<title>By: T. Ryan Gregory</title>
		<link>http://www.genomicron.evolverzone.com/2009/12/the-junk-dna-myth-or-lack-thereof-explained-one-more-time/comment-page-1/#comment-1553</link>
		<dc:creator>T. Ryan Gregory</dc:creator>
		<pubDate>Mon, 07 Jun 2010 16:59:22 +0000</pubDate>
		<guid isPermaLink="false">http://www.genomicron.evolverzone.com/?p=703#comment-1553</guid>
		<description>Scientists may often be described as baffled, but we actually aren&#039;t so confused about this question.</description>
		<content:encoded><![CDATA[<p>Scientists may often be described as baffled, but we actually aren&#8217;t so confused about this question.</p>
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		<title>By: MTiffany</title>
		<link>http://www.genomicron.evolverzone.com/2009/12/the-junk-dna-myth-or-lack-thereof-explained-one-more-time/comment-page-1/#comment-1552</link>
		<dc:creator>MTiffany</dc:creator>
		<pubDate>Mon, 07 Jun 2010 16:13:22 +0000</pubDate>
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		<description>Instead of &quot;junk&quot; DNA, how about we refer to it as &quot;baffling&quot; DNA, is in, we&#039;re baffled as to what particular stretches of the genome do?</description>
		<content:encoded><![CDATA[<p>Instead of &#8220;junk&#8221; DNA, how about we refer to it as &#8220;baffling&#8221; DNA, is in, we&#8217;re baffled as to what particular stretches of the genome do?</p>
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		<title>By: Keith Grimaldi</title>
		<link>http://www.genomicron.evolverzone.com/2009/12/the-junk-dna-myth-or-lack-thereof-explained-one-more-time/comment-page-1/#comment-1356</link>
		<dc:creator>Keith Grimaldi</dc:creator>
		<pubDate>Mon, 14 Dec 2009 16:15:09 +0000</pubDate>
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		<description> 
&lt;blockquote cite=&quot;comment-1349&quot;&gt;&lt;strong&gt;&lt;a href=&quot;#comment-1349&quot; rel=&quot;nofollow&quot;&gt;T. Ryan Gregory&lt;/a&gt;&lt;/strong&gt;:   I think your comments are on the right track, but the one quoted here is problematic.  It is not the case that this idea is held as the explanation until it is refuted when there is no supporting evidence.  The burden of proof is on proponents to show why this idea should continue to be taken seriously.&lt;/blockquote&gt;
Yes - here I mean that more complex theories should not be proposed in preference unless there is good evidence for them - of course that is exactly what I have been doing with protective vs. null, as explained in the other post on your later edition of the junk story!
 </description>
		<content:encoded><![CDATA[<p> </p>
<blockquote cite="comment-1349"><p><strong><a href="#comment-1349" rel="nofollow">T. Ryan Gregory</a></strong>:   I think your comments are on the right track, but the one quoted here is problematic.  It is not the case that this idea is held as the explanation until it is refuted when there is no supporting evidence.  The burden of proof is on proponents to show why this idea should continue to be taken seriously.</p></blockquote>
<p>Yes &#8211; here I mean that more complex theories should not be proposed in preference unless there is good evidence for them &#8211; of course that is exactly what I have been doing with protective vs. null, as explained in the other post on your later edition of the junk story!<br />
 </p>
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		<title>By: T. Ryan Gregory</title>
		<link>http://www.genomicron.evolverzone.com/2009/12/the-junk-dna-myth-or-lack-thereof-explained-one-more-time/comment-page-1/#comment-1351</link>
		<dc:creator>T. Ryan Gregory</dc:creator>
		<pubDate>Mon, 14 Dec 2009 13:25:56 +0000</pubDate>
		<guid isPermaLink="false">http://www.genomicron.evolverzone.com/?p=703#comment-1351</guid>
		<description>&lt;p&gt; &lt;/p&gt;
&lt;blockquote cite=&quot;comment-1347&quot;&gt;&lt;strong&gt;&lt;a href=&quot;#comment-1347&quot; rel=&quot;nofollow&quot;&gt;Keith Grimaldi&lt;/a&gt;&lt;/strong&gt;: find a long lived species with no “junk”;&lt;/blockquote&gt;
&lt;p&gt;&quot;No junk&quot; is a pretty strict requirement, but here&#039;s an interesting one.  The red sea urchin, &lt;em&gt;Strongylocentrotus franciscanus&lt;/em&gt;, has been &lt;a href=&quot;http://www.vetmed.ucdavis.edu/whc/seadoc/pdfs/urchinlongevity.pdf&quot; rel=&quot;nofollow&quot;&gt;reported to live up to 100 years&lt;/a&gt;.  It has an &lt;a href=&quot;http://www.genomesize.com/result_species.php?id=1607&quot; rel=&quot;nofollow&quot;&gt;estimated genome size&lt;/a&gt; of only about 800Mb.&lt;/p&gt;
&lt;p&gt; &lt;/p&gt;
&lt;p&gt; &lt;/p&gt;
&lt;p&gt; &lt;/p&gt;
&lt;p&gt; &lt;/p&gt;</description>
		<content:encoded><![CDATA[<p> </p>
<blockquote cite="comment-1347"><p><strong><a href="#comment-1347" rel="nofollow">Keith Grimaldi</a></strong>: find a long lived species with no “junk”;</p></blockquote>
<p>&#8220;No junk&#8221; is a pretty strict requirement, but here&#8217;s an interesting one.  The red sea urchin, <em>Strongylocentrotus franciscanus</em>, has been <a href="http://www.vetmed.ucdavis.edu/whc/seadoc/pdfs/urchinlongevity.pdf" rel="nofollow">reported to live up to 100 years</a>.  It has an <a href="http://www.genomesize.com/result_species.php?id=1607" rel="nofollow">estimated genome size</a> of only about 800Mb.</p>
<p> </p>
<p> </p>
<p> </p>
<p> </p>
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		<title>By: T. Ryan Gregory</title>
		<link>http://www.genomicron.evolverzone.com/2009/12/the-junk-dna-myth-or-lack-thereof-explained-one-more-time/comment-page-1/#comment-1349</link>
		<dc:creator>T. Ryan Gregory</dc:creator>
		<pubDate>Mon, 14 Dec 2009 13:04:05 +0000</pubDate>
		<guid isPermaLink="false">http://www.genomicron.evolverzone.com/?p=703#comment-1349</guid>
		<description>&lt;p&gt; &lt;/p&gt;
&lt;blockquote cite=&quot;comment-1347&quot;&gt;&lt;strong&gt;&lt;a href=&quot;#comment-1347&quot; rel=&quot;nofollow&quot;&gt;Keith Grimaldi&lt;/a&gt;&lt;/strong&gt;: It just seems to be one of the simplest explanations that should be dismissed (with evidence) before proposing more complex hypotheses (without real evidence).&lt;/blockquote&gt;
&lt;p&gt;I think your comments are on the right track, but the one quoted here is problematic.  It is not the case that this idea is held as the explanation until it is refuted when there is no supporting evidence.  The burden of proof is on proponents to show why this idea should continue to be taken seriously.&lt;/p&gt;
&lt;p&gt; &lt;/p&gt;
&lt;p&gt; &lt;/p&gt;</description>
		<content:encoded><![CDATA[<p> </p>
<blockquote cite="comment-1347"><p><strong><a href="#comment-1347" rel="nofollow">Keith Grimaldi</a></strong>: It just seems to be one of the simplest explanations that should be dismissed (with evidence) before proposing more complex hypotheses (without real evidence).</p></blockquote>
<p>I think your comments are on the right track, but the one quoted here is problematic.  It is not the case that this idea is held as the explanation until it is refuted when there is no supporting evidence.  The burden of proof is on proponents to show why this idea should continue to be taken seriously.</p>
<p> </p>
<p> </p>
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		<title>By: Keith Grimaldi</title>
		<link>http://www.genomicron.evolverzone.com/2009/12/the-junk-dna-myth-or-lack-thereof-explained-one-more-time/comment-page-1/#comment-1347</link>
		<dc:creator>Keith Grimaldi</dc:creator>
		<pubDate>Mon, 14 Dec 2009 11:07:29 +0000</pubDate>
		<guid isPermaLink="false">http://www.genomicron.evolverzone.com/?p=703#comment-1347</guid>
		<description>Estimates of endogenous oxidative damage (8-hydroxydeoxyguanosine) range from a low end of 100 events per cell per day to 10,000 per day. Multiplied by trillions of cells coupled with the not 100% fidelity of DNA repair mechanisms mean that mutation is not a rare event. DNA damage limitation is very important for human aging as seen in the cases of the various DNA repair deficiency diseases (XP, Cockayne’s, etc). DNA is a target for oxidative damage, reducing the size of the genome e.g. by 50% would not reduce the amount of oxidative damage by 50% but would increase the levels of damage on the remaining genome (mitochondrial DNA is very small but has high damage rates, even accounting for the oxidative reactions taking place locally.
 Testable hypotheses are not so easy but i suppose there are some. It’s not of course my theory, that would be ridiculous to propose, it’s something that has been going around for ages (not surprising as it’s an obvious possibility) and does not yet seem to have been refuted. It just seems to be one of the simplest explanations that should be dismissed (with evidence) before proposing more complex hypotheses (without real evidence). It has been discussed by many others, including more recently – Patrushev, 2006, Russian Journal of Bioorganic Chemistry, Volume 32, Number 4 / July, 2006.

1. No significant lifespan is possible with a sequence dependent functional only genome - I don&#039;t know offhand what &quot;significant&quot; is, but at least  it would predict that in any creature living for more than few years the genome will be mainly &quot;junk&quot;, or not sequence sensitive

2. If the bulk of DNA is &quot;junk&quot; then sequence preservation will not be important and will not be conserved. Take some skin fibroblasts from an individual and make monoclonal cultures from them, sequence and compare coding vs &quot;junk&quot; regions to compare mutation rates in different genome areas between different cells from a single individual. This will be possible in the not too distant future with &quot;next-next&quot; gen sequencing (whole genome in sequenced in 15 mins!). For now maybe it could be speeded up a bit by culturing in a mutagenic medium and sequencing long stretches rather than whole genome. 
3. Mitochondrial DNA will not need protection because of the number of copies per cell. Random mutations will not become established, just like a single strain of e.coli will remain the same strain unless selective pressure is applied

4. Removal of large portions of non-sequence conserved &quot;junk&quot; DNA should shorten life span - this i suppose would be technically tricky

5. Refutation – any of the following: 
a) find a long lived species with no &quot;junk&quot;;
b) show that majority of DNA is highly sequence sensitive; 
c) removing &quot;junk&quot; has no effect on damage induced aging;
d) explain how a “coding only” genome could sustain mitochondrial levels of damage;
e) demonstrate other functions for the majority of the non-coding DNA;

Chris Lawson: &quot;I think that long stretches of non-coding DNA will increase the chances of higher-level replication errors (e.g. Fragile X syndrome, Down syndrome).  &quot;  OK, but does it really? and does it increase mutation or are the errors detected and cells killed by apoptosis

Who moved the goalposts and where by the way??
 </description>
		<content:encoded><![CDATA[<p>Estimates of endogenous oxidative damage (8-hydroxydeoxyguanosine) range from a low end of 100 events per cell per day to 10,000 per day. Multiplied by trillions of cells coupled with the not 100% fidelity of DNA repair mechanisms mean that mutation is not a rare event. DNA damage limitation is very important for human aging as seen in the cases of the various DNA repair deficiency diseases (XP, Cockayne’s, etc). DNA is a target for oxidative damage, reducing the size of the genome e.g. by 50% would not reduce the amount of oxidative damage by 50% but would increase the levels of damage on the remaining genome (mitochondrial DNA is very small but has high damage rates, even accounting for the oxidative reactions taking place locally.<br />
 Testable hypotheses are not so easy but i suppose there are some. It’s not of course my theory, that would be ridiculous to propose, it’s something that has been going around for ages (not surprising as it’s an obvious possibility) and does not yet seem to have been refuted. It just seems to be one of the simplest explanations that should be dismissed (with evidence) before proposing more complex hypotheses (without real evidence). It has been discussed by many others, including more recently – Patrushev, 2006, Russian Journal of Bioorganic Chemistry, Volume 32, Number 4 / July, 2006.</p>
<p>1. No significant lifespan is possible with a sequence dependent functional only genome &#8211; I don&#8217;t know offhand what &#8220;significant&#8221; is, but at least  it would predict that in any creature living for more than few years the genome will be mainly &#8220;junk&#8221;, or not sequence sensitive</p>
<p>2. If the bulk of DNA is &#8220;junk&#8221; then sequence preservation will not be important and will not be conserved. Take some skin fibroblasts from an individual and make monoclonal cultures from them, sequence and compare coding vs &#8220;junk&#8221; regions to compare mutation rates in different genome areas between different cells from a single individual. This will be possible in the not too distant future with &#8220;next-next&#8221; gen sequencing (whole genome in sequenced in 15 mins!). For now maybe it could be speeded up a bit by culturing in a mutagenic medium and sequencing long stretches rather than whole genome.<br />
3. Mitochondrial DNA will not need protection because of the number of copies per cell. Random mutations will not become established, just like a single strain of e.coli will remain the same strain unless selective pressure is applied</p>
<p>4. Removal of large portions of non-sequence conserved &#8220;junk&#8221; DNA should shorten life span &#8211; this i suppose would be technically tricky</p>
<p>5. Refutation – any of the following:<br />
a) find a long lived species with no &#8220;junk&#8221;;<br />
b) show that majority of DNA is highly sequence sensitive;<br />
c) removing &#8220;junk&#8221; has no effect on damage induced aging;<br />
d) explain how a “coding only” genome could sustain mitochondrial levels of damage;<br />
e) demonstrate other functions for the majority of the non-coding DNA;</p>
<p>Chris Lawson: &#8220;I think that long stretches of non-coding DNA will increase the chances of higher-level replication errors (e.g. Fragile X syndrome, Down syndrome).  &#8221;  OK, but does it really? and does it increase mutation or are the errors detected and cells killed by apoptosis</p>
<p>Who moved the goalposts and where by the way??<br />
 </p>
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		<title>By: T. Ryan Gregory</title>
		<link>http://www.genomicron.evolverzone.com/2009/12/the-junk-dna-myth-or-lack-thereof-explained-one-more-time/comment-page-1/#comment-1345</link>
		<dc:creator>T. Ryan Gregory</dc:creator>
		<pubDate>Sun, 13 Dec 2009 22:09:13 +0000</pubDate>
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		<description>It&#039;s not just (or probably even mainly) S-phase that is impacted.</description>
		<content:encoded><![CDATA[<p>It&#8217;s not just (or probably even mainly) S-phase that is impacted.</p>
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		<title>By: Earrnz</title>
		<link>http://www.genomicron.evolverzone.com/2009/12/the-junk-dna-myth-or-lack-thereof-explained-one-more-time/comment-page-1/#comment-1344</link>
		<dc:creator>Earrnz</dc:creator>
		<pubDate>Sun, 13 Dec 2009 21:44:26 +0000</pubDate>
		<guid isPermaLink="false">http://www.genomicron.evolverzone.com/?p=703#comment-1344</guid>
		<description>Darn, you&#039;re right about the replication origins. Yet, quoting Ryan himself:
&lt;em&gt;More generally, it has been known for more than 50 years that the total quantity of DNA in the genome is linked to nucleus size, cell size, cell division rate, and a wide range of organism-level characteristics that derive from these cytological features.&lt;/em&gt;
&lt;a title=&quot;Entry&quot; href=&quot;../../../2008/02/non-functional-dna-non-functional-vs/&quot; rel=&quot;nofollow&quot;&gt;http://www.genomicron.evolverzone.com/2008/02/non-functional-dna-non-functional-vs/&lt;/a&gt;
So genome size seems to have an effect on cell cycle duration, or at least, it was said so. What would that effect be?</description>
		<content:encoded><![CDATA[<p>Darn, you&#8217;re right about the replication origins. Yet, quoting Ryan himself:<br />
<em>More generally, it has been known for more than 50 years that the total quantity of DNA in the genome is linked to nucleus size, cell size, cell division rate, and a wide range of organism-level characteristics that derive from these cytological features.</em><br />
<a title="Entry" href="../../../2008/02/non-functional-dna-non-functional-vs/" rel="nofollow">http://www.genomicron.evolverzone.com/2008/02/non-functional-dna-non-functional-vs/</a><br />
So genome size seems to have an effect on cell cycle duration, or at least, it was said so. What would that effect be?</p>
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		<title>By: Chris Lawson</title>
		<link>http://www.genomicron.evolverzone.com/2009/12/the-junk-dna-myth-or-lack-thereof-explained-one-more-time/comment-page-1/#comment-1343</link>
		<dc:creator>Chris Lawson</dc:creator>
		<pubDate>Sun, 13 Dec 2009 09:50:01 +0000</pubDate>
		<guid isPermaLink="false">http://www.genomicron.evolverzone.com/?p=703#comment-1343</guid>
		<description>I think Keith&#039;s understanding is that there are a set number of mutations per cell and therefore more &quot;junk DNA&quot; means fewer of those mutations will take place in functional genes. Not only do I find this unconvincing, I think that long stretches of non-coding DNA will increase the chances of higher-level replication errors (e.g. Fragile X syndrome, Down syndrome).</description>
		<content:encoded><![CDATA[<p>I think Keith&#8217;s understanding is that there are a set number of mutations per cell and therefore more &#8220;junk DNA&#8221; means fewer of those mutations will take place in functional genes. Not only do I find this unconvincing, I think that long stretches of non-coding DNA will increase the chances of higher-level replication errors (e.g. Fragile X syndrome, Down syndrome).</p>
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		<title>By: T. Ryan Gregory</title>
		<link>http://www.genomicron.evolverzone.com/2009/12/the-junk-dna-myth-or-lack-thereof-explained-one-more-time/comment-page-1/#comment-1342</link>
		<dc:creator>T. Ryan Gregory</dc:creator>
		<pubDate>Sat, 12 Dec 2009 14:38:41 +0000</pubDate>
		<guid isPermaLink="false">http://www.genomicron.evolverzone.com/?p=703#comment-1342</guid>
		<description>&lt;p&gt;The goalposts are moving so fast, I&#039;m not even sure where they stand now.  Why don&#039;t you provide the following, and we&#039;ll go from there:&lt;/p&gt;
&lt;p&gt;1) What &lt;em&gt;specific&lt;/em&gt;, testable predictions does your hypothesis make?&lt;/p&gt;
&lt;p&gt;2) What evidence would you accept as refuting the hypothesis?&lt;/p&gt;
&lt;p&gt; &lt;/p&gt;</description>
		<content:encoded><![CDATA[<p>The goalposts are moving so fast, I&#8217;m not even sure where they stand now.  Why don&#8217;t you provide the following, and we&#8217;ll go from there:</p>
<p>1) What <em>specific</em>, testable predictions does your hypothesis make?</p>
<p>2) What evidence would you accept as refuting the hypothesis?</p>
<p> </p>
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