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    <title>Nature Precedings - Shi Huang</title>
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    <description>Documents posted by Shi Huang</description>
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    <dc:language>en</dc:language>
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      <title>Primate phylogeny: molecular evidence for a pongid clade excluding humans and a prosimian clade containing tarsiers </title>
      <link>http://precedings.nature.com/documents/3794/version/1</link>
      <description>Interpretations of molecular data by the modern evolution theory are often sharply inconsistent with paleontological results.  This is to be expected since the theory is only true for microevolution and yet fossil records are mostly about macroevolution.  The maximum genetic diversity (MGD) hypothesis is a more coherent and complete account of evolution that has yet to meet a single contradiction.  Here, molecular data were analyzed based on the MGD to resolve key questions of primate phylogeny.  A new method was developed from a novel result predicted by the MGD: genetic non-equidistance to a simpler taxon only in slow but not in fast evolving sequences given non-equidistance in time.  This &#8216;slow clock&#8217; method showed that humans are genetically more distant to orangutans than African apes are and separated from the pongid clade (containing orangutan and African apes) 17.3 million years ago.  Also, tarsiers are genetically closer to lorises than simian primates are, suggesting a tarsier-loris clade to the exclusion of simian primates.  The validity and internal coherence of the primate phylogeny here were independently verified.  The molecular split time of human and pongid calibrated from the fossil record of gorilla, or the fossil times for the radiation of anthropoids/mammals at the K/T boundary and for the Eutheria-Metatheria split in the Early Cretaceous, were independently confirmed from molecular dating calibrated using the fossil split times of tarsier-loris and two other pairs of mammals (mouse-rat and opossum-kangaroo).  This remarkable and unprecedented concordance between molecules and fossils provides the latest confirmation of the inseparable unity of genotype and phenotype and the unmatched value of MGD in a coherent interpretation of life history.  </description>
      <guid>http://precedings.nature.com/documents/3794/version/1</guid>
      <pubDate>Tue, 22 Sep 2009 16:42:20 UTC</pubDate>
      <dc:title>Primate phylogeny: molecular evidence for a pongid clade excluding humans and a prosimian clade containing tarsiers </dc:title>
      <dc:identifier>hdl:10101/npre.2009.3794.1</dc:identifier>
      <dc:date>2009-09-22</dc:date>
      <dc:creator>Shi Huang</dc:creator>
      <prism:publicationName>Nature Precedings</prism:publicationName>
      <prism:publicationDate>2009-09-22T16:42:20Z</prism:publicationDate>
      <prism:category>Manuscript</prism:category>
      <prism:section>Bioinformatics</prism:section>
      <prism:section>Evolutionary Biology</prism:section>
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      <title>Molecular evidence for the hadrosaur B. canadensis as an outgroup to a clade containing the dinosaur T. rex and birds</title>
      <link>http://precedings.nature.com/documents/3255/version/1</link>
      <description>Molecular analysis of collagen sequences from an 80 million year old hadrosaur B. canadensis and a 68 million year old dinosaur T. rex suggest strongly that B. canadensis is an outgroup to a clade containing T. rex and birds, fully consistent with the well-established phylogeny based on morphological analyses of fossils.  </description>
      <guid>http://precedings.nature.com/documents/3255/version/1</guid>
      <pubDate>Wed, 27 May 2009 14:55:41 UTC</pubDate>
      <dc:title>Molecular evidence for the hadrosaur B. canadensis as an outgroup to a clade containing the dinosaur T. rex and birds</dc:title>
      <dc:identifier>hdl:10101/npre.2009.3255.1</dc:identifier>
      <dc:date>2009-05-27</dc:date>
      <dc:creator>Shi Huang</dc:creator>
      <prism:publicationName>Nature Precedings</prism:publicationName>
      <prism:publicationDate>2009-05-27T14:55:41Z</prism:publicationDate>
      <prism:category>Manuscript</prism:category>
      <prism:section>Bioinformatics</prism:section>
      <prism:section>Evolutionary Biology</prism:section>
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      <title>Inverse relationship between genetic diversity and epigenetic complexity</title>
      <link>http://dx.doi.org/10.1038/npre.2009.1751.2</link>
      <description>Early studies of molecular evolution revealed a correlation between genetic distance and time of species divergence.  This observation provoked the molecular clock hypothesis and in turn the &#8216;Neutral Theory&#8217;, which however remains an incomplete explanation since it predicts a constant mutation rate per generation whereas empirical evidence suggests a constant rate per year.  Data inconsistent with the molecular clock hypothesis have steadily accumulated in recent years that show no correlation between genetic distance and time of divergence.  It has therefore become a challenge to find a testable idea that can reconcile the seemingly conflicting data sets.  Here, an inverse relationship between genetic diversity and epigenetic complexity was deduced from a simple intuition in building complex systems.  Genetic diversity, i.e., genetic distance or dissimilarity in DNA or protein sequences between individuals or species, is restricted by the complexity of epigenetic programs.  This inverse relationship logically deduces the maximum genetic diversity (MGD) hypothesis, which suggests that macroevolution from simple to complex organisms involves a punctuational increase in epigenetic complexity that in turn causes a punctuational loss in genetic diversity.  The hypothesis fully grants Neo-Darwinism to be what it really is (a theory of microevolution) and explains all the major facts of evolution.  Importantly, it predicts the most remarkable result of molecular evolution, the genetic equidistance result, which originally provoked the molecular clock hypothesis.</description>
      <guid>http://dx.doi.org/10.1038/npre.2009.1751.2</guid>
      <pubDate>Thu, 15 Jan 2009 15:25:06 UTC</pubDate>
      <dc:title>Inverse relationship between genetic diversity and epigenetic complexity</dc:title>
      <dc:identifier>doi:10.1038/npre.2009.1751.2</dc:identifier>
      <dc:date>2009-01-15</dc:date>
      <dc:creator>Shi Huang</dc:creator>
      <prism:publicationName>Nature Precedings</prism:publicationName>
      <prism:publicationDate>2009-01-15T15:25:06Z</prism:publicationDate>
      <prism:category>Manuscript</prism:category>
      <prism:section>Genetics &amp; Genomics</prism:section>
      <prism:section>Bioinformatics</prism:section>
      <prism:section>Evolutionary Biology</prism:section>
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      <title>The genetic equidistance result of molecular evolution is independent of mutation rates</title>
      <link>http://precedings.nature.com/documents/1733/version/3</link>
      <description>The well-established genetic equidistance result shows that sister species are approximately equidistant to a simpler outgroup as measured by DNA or protein dissimilarity.  The equidistance result is the most direct evidence, and remains the only evidence, for the constant mutation rate interpretation of this result, known as the molecular clock.  However, data independent of the equidistance result have steadily accumulated in recent years that often violate a constant mutation rate.  Many have automatically inferred non-equidistance whenever a non-constant mutation rate was observed, based on the unproven assumption that the equidistance result is an outcome of constant mutation rate.  Here it is shown that the equidistance result remains valid even when different species can be independently shown to have different mutation rates.  A random sampling of 50 proteins shows that nearly all proteins display the equidistance result despite the fact that many proteins have non-constant mutation rates.  Therefore, the genetic equidistance result does not necessarily mean a constant mutation rate.  Observations of different mutation rates do not invalidate the genetic equidistance result.  New ideas are needed to explain the genetic equidistance result that must grant different mutation rates to different species and must be independently testable.  </description>
      <guid>http://precedings.nature.com/documents/1733/version/3</guid>
      <pubDate>Tue, 25 Nov 2008 17:42:42 UTC</pubDate>
      <dc:title>The genetic equidistance result of molecular evolution is independent of mutation rates</dc:title>
      <dc:identifier>hdl:10101/npre.2008.1733.3</dc:identifier>
      <dc:date>2008-11-25</dc:date>
      <dc:creator>Shi Huang</dc:creator>
      <prism:publicationName>Nature Precedings</prism:publicationName>
      <prism:publicationDate>2008-11-25T17:42:42Z</prism:publicationDate>
      <prism:category>Manuscript</prism:category>
      <prism:section>Ecology</prism:section>
      <prism:section>Genetics &amp; Genomics</prism:section>
      <prism:section>Bioinformatics</prism:section>
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      <title>Ancient fossil specimens of extinct species are genetically more distant to an outgroup than extant sister species are</title>
      <link>http://precedings.nature.com/documents/1676/version/2</link>
      <description>There exists a remarkable correlation between genetic distance as measured by protein or DNA dissimilarity and time of species divergence as inferred from fossil records.  This observation has provoked the molecular clock hypothesis. However, data inconsistent with the hypothesis have steadily accumulated in recent years from studies of extant organisms.  Here the published DNA and protein sequences from ancient fossil specimens were examined to see if they would support the molecular clock hypothesis.  The hypothesis predicts that ancient specimens cannot be genetically more distant to an outgroup than extant sister species are.  Also, two distinct ancient specimens cannot be genetically more distant than their extant sister species are.  The findings here do not conform to these predictions.  Neanderthals are more distant to chimpanzees and gorillas than modern humans are.  Dinosaurs are more distant to frogs than extant birds are.  Mastodons are more distant to opossums than other placental mammals are.  The genetic distance between dinosaurs and mastodons is greater than that between extant birds and mammals. Therefore, while the molecular clock hypothesis is consistent with some data from extant organisms, it has yet to find support from ancient fossils. Far more damaging to the hypothesis than data from extant organisms, which merely question the constancy of mutation rate, the study of ancient fossil organisms here challenges for the first time the fundamental premise of modern evolution theory that genetic distances had always increased with time in the past history of life on Earth.</description>
      <guid>http://precedings.nature.com/documents/1676/version/2</guid>
      <pubDate>Fri, 25 Jul 2008 15:02:55 UTC</pubDate>
      <dc:title>Ancient fossil specimens of extinct species are genetically more distant to an outgroup than extant sister species are</dc:title>
      <dc:identifier>hdl:10101/npre.2008.1676.2</dc:identifier>
      <dc:date>2008-07-25</dc:date>
      <dc:creator>Shi Huang</dc:creator>
      <prism:publicationName>Nature Precedings</prism:publicationName>
      <prism:publicationDate>2008-07-25T15:02:55Z</prism:publicationDate>
      <prism:category>Manuscript</prism:category>
      <prism:section>Bioinformatics</prism:section>
      <prism:section>Evolutionary Biology</prism:section>
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      <title>Requirement of RIZ1 for cancer prevention by methyl-balanced diet</title>
      <link>http://precedings.nature.com/documents/1732/version/1</link>
      <description>The typical Western diet is not balanced in methyl nutrients that regulate the level of the methyl donor S-adenosylmethionine (SAM) and its derivative metabolite S-adenosylhomocysteine (SAH), which in turn may control the activity of certain methyltransferases.  Feeding rodents with amino acid defined and methyl-imbalanced diet decreases hepatic SAM and causes liver cancers. RIZ1 (PRDM2 or KMT8) is a tumor suppressor and functions in transcriptional repression by methylating histone H3 lysine 9.  Here we show that a methyl-balanced diet conferred additional survival benefits compared to a tumor-inducing methyl-imbalanced diet only in mice with wild type RIZ1 but not in mice deficient in RIZ1.  While absence of RIZ1 was tumorigenic in mice fed the balanced diet, its presence did not prevent tumor formation in mice fed the imbalanced diet.  Unlike most of its related enzymes, RIZ1 was upregulated by methyl-balanced diet.  Methyl-balanced diet did not fully repress oncogenes such as c-Jun in the absence of RIZ1.  The data identify RIZ1 as a critical target of methyl-balanced diet in cancer prevention.  The molecular understanding of dietary carcinogenesis may help people make informed choices on diet, which may greatly reduce the incidence of cancer.      </description>
      <guid>http://precedings.nature.com/documents/1732/version/1</guid>
      <pubDate>Fri, 28 Mar 2008 16:30:31 UTC</pubDate>
      <dc:title>Requirement of RIZ1 for cancer prevention by methyl-balanced diet</dc:title>
      <dc:identifier>hdl:10101/npre.2008.1732.1</dc:identifier>
      <dc:date>2008-03-28</dc:date>
      <dc:creator>Shi Huang </dc:creator>
      <prism:publicationName>Nature Precedings</prism:publicationName>
      <prism:publicationDate>2008-03-28T16:30:31Z</prism:publicationDate>
      <prism:category>Manuscript</prism:category>
      <prism:section>Cancer</prism:section>
      <prism:section>Genetics &amp; Genomics</prism:section>
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