Showing posts with label MGD. Show all posts
Showing posts with label MGD. Show all posts

Sunday, June 26, 2016

Species biology as major determinants of genetic diversity

I recently found a Nature paper: Comparative population genomics in animals uncovers the determinants of genetic diversity  reporting findings on determinants of genetic diversity, which is well anticipated by the MGD theory.

The authors said:"Our analysis reveals that polymorphism levels are well predicted by species biology, whereas historical and contingent factors are only minor determinants of the genetic diversity of a species."

So, as we have said all along since 2008, genetic diversity in most cases have nothing to do with effective population size or bottle necks. It is largely determined by species complexity, which is the most important aspect of species biology. 

It is really great and satisfying to see that others have independently come to our point of view, even though they have yet to fully acknowledge our series of papers published since 2008.

References:






Monday, June 20, 2016

Genomics: Special issue on the comprehensive functionality of genomic DNA

Genomics special issue to dump the junk DNA notion to junk yards

#genomics #genetics Editorial: Special issue on the comprehensive functionality of ge... https://t.co/9FtaDo9IZthttps://t.co/oR40nVo503

From the editorial by Huang: “About 80% of the human genome are transcribed but how much of it is functional is under hot debate. As one would immediately know if one takes an honest look at all the facts, the junk DNA position really is just hot air: it is neither supported by facts nor by axioms or self-evident logical reasoning, and has already been falsified by the failure of the universal molecular clock hypothesis. In fact, the exact opposite of neutrality should now become the null hypothesis because it is free of factual contradictions and accounts for all known facts.”


Thursday, October 22, 2015

New thoughts on an old riddle: what determines genetic diversity within and between species?



The abstract and the introduction section of the paper are posted below.


Abstract

The question of what determines genetic diversity both between and within species has long remained unsolved by the modern evolutionary theory (MET). However, it has not deterred researchers from producing interpretations of genetic diversity by using MET. We here examine the two key experimental observations of genetic diversity made in the 1960s, one between species and the other within a population of a species, that directly contributed to the development of MET. The interpretations of these observations as well as the assumptions by MET are widely known to be inadequate. We review the recent progress of an alternative framework, the maximum genetic diversity (MGD) hypothesis, that uses axioms and natural selection to explain the vast majority of genetic diversity as being at optimum equilibrium that is largely determined by organismal complexity. The MGD hypothesis fully absorbs the proven virtues of MET and considers its assumptions relevant only to a much more limited scope. This new synthesis has accounted for the much overlooked phenomenon of progression towards higher complexity, and more importantly, been instrumental in directing productive research into both evolutionary and biomedical problems.   


Introduction

The modern evolutionary theory (MET) consists of Darwin’s theory of natural selection and Kimura’s Neutral theory (also Ohta’s Nearly Neutral theory). The theory treats evolution the same as population genetics. The Darwinian theory is much better known than the Neutral theory. However, for molecular evolution and population genetics, the Neutral theory (and the Nearly Neutral theory) has been more useful. Regardless, however, the MET is still incomplete, as acknowledged by Ohta and Gillespie: "..we have yet to find a mechanistic theory of molecular evolution that can readily account for all of the phenomenology. ..we would like to call attention to a looming crisis as theoretical investigations lag behind the phenomenology." [1].


Key puzzles of evolution remain unsolved by the MET. The central problem of the field is and has always been the old riddle of what determines genetic diversity [2-5]. Is it mostly determined by natural selection or neutral drift? Here we critically examine the historical origins and assumptions of the MET. We show that both the neutral and the selection frameworks were largely mistaken right from the beginning. Key observations that directly inspired the neutral theory were nearly half of a century ahead of their time. Selection schemes on the other hand was largely influenced by the one gene one trait genetics of the early 1900s and always treated single locus as the target of selection, which is in fact rarely the case for most of the commonly observed variations as recent studies have shown [6-11]. Finally, we review a candidate for superseding the MET, the maximum genetic diversity (MGD) hypothesis first published in 2008 [12,13], that fully absorbs the proven virtues of the MET and has more explanatory power as well as greater value in directing productive research in a much wider field of biomedical science [6-11,14]. The old riddle of genetic diversity within and between species is solved as mere deductions of the assumptions of the MGD. Only in this case, the assumptions are, for the first time in biology, self-evident intuitions that are no less true or false than any known axioms of hard sciences or mathematics.


References:
1. Ohta T, Gillespie JH (1996) Development of Neutral and Nearly Neutral Theories. Theor Popul Biol 49: 128-142.
2. Leffler EM, Bullaughey K, Matute DR, Meyer WK, Segurel L, et al. (2012) Revisiting an old riddle: what determines genetic diversity levels within species? PLoS Biol 10: e1001388.
3. Aquadro CF (1992) Why is the genome variable? Insights from Drosophila. Trends Genet 8: 355-362.
4. Lewontin RC (1991) Twenty-five years ago in Genetics: electrophoresis in the development of evolutionary genetics: milestone or millstone? Genetics 128: 657-662.
5. Lewontin RC (1974) The genetic basis of evolutionary change. New York and London: Columbia University Press.
6. Yuan D, Zhu Z, Tan X, Liang J, Zeng C, et al. (2014) Scoring the collective effects of SNPs: association of minor alleles with complex traits in model organisms. Sci China Life Sci 57: 876-888.
7. Zhu Z, Man X, Xia M, Huang Y, Yuan D, et al. (2015) Collective effects of SNPs on transgenerational inheritance in Caenorhabditis elegans and budding yeast. Genomics 106: 23-29.
8. Zhu Z, Yuan D, Luo D, Lu X, Huang S (2015) Enrichment of Minor Alleles of Common SNPs and Improved Risk Prediction for Parkinson's Disease. PLoS ONE 10: e0133421.
9. Yuan D, Zhu Z, Tan X, Liang J, Zeng C, et al. (2012) Minor alleles of common SNPs quantitatively affect traits/diseases and are under both positive and negative selection. arXiv:12092911.
10. Zhu Z, Lu Q, Zeng F, Wang J, Huang S (2015) Compatibility between mitochondrial and nuclear genomes correlates wtih quantitative trait of lifespan in Caenorhabditis elegans. Sci Rep: in press.
11. Zhu Z, Lu Q, Wang J, Huang S (2015) Collective effects of common SNPs in foraging decisions in Caenorhabditis elegans and an integrative method of identification of candidate genes. Sci Rep: in press.
12. Huang S (2009) Inverse relationship between genetic diversity and epigenetic complexity. Preprint available at Nature Precedings <http://dx.doi.org/10.1038/npre.2009.1751.2>
13. Huang S (2008) Histone methylation and the initiation of cancer, Cancer Epigenetics; Tollefsbol T, editor. New York: CRC Press.

14. Huang S (2012) Primate phylogeny: molecular evidence for a pongid clade excluding humans and a prosimian clade containing tarsiers. Sci China Life Sci 55: 709-725.