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Mutational hazard hypothesis

The mutational hazard hypothesis is a non-adaptive theory for increased complexity in genomes.[1] The basis of mutational hazard hypothesis is that each mutation for non-coding DNA imposes a fitness cost.[2] Variation in complexity can be described by 2Neu, where Ne is effective population size and u is mutation rate.[3]

In this hypothesis, selection against non-coding DNA can be reduced in three ways: random genetic drift, recombination rate, and mutation rate.[4] As complexity increases from prokaryotes to multicellular eukaryotes, effective population size decreases, subsequently increasing the strength of random genetic drift[1]. This, along with low recombination rate[4] and high mutation rate[4], allows non-coding DNA to proliferate without being removed by purifying selection.[1]

Accumulation of non-coding DNA in larger genomes can be seen when comparing genome size and genome content across eukaryotic taxa. There is a positive correlation between genome size and noncoding DNA genome content with each group staying within some variation.[1][2] When comparing variation in complexity in organelles, effective population size is replaced with genetic effective population size (Ng).[3] In plant and animal mitochondria, differences in mutation rate account for the opposite directions in complexity, with plant mitochondria being more complex and animal mitochondria more streamlined.[5]

The mutational hazard hypothesis has been used to explain the differences between mitochondrial, nuclear, and plastid genomes in Volvox cateri.[6] However a later study found that Volvox cateri and Volvox africanus have a higher intergenic mutation rate in their plastid genomes.[7] The hypothesis was also used as a possible explanation for intron loss and compact genome site in Arabiopsis thaliana. When compared to Arabidopsis lyrata, researchers found a higher mutation rate overall and in lost introns compared to conserved introns.[8]

Mitochondrial genomes in Seline noctiflora and Seline conica only partially lined up with the mutational hazard hypothesis. Even though they have lower intron lengths and more non-coding DNA elements, their higher mutation rate and genome expansion is opposite of what the hypothesis predicts.[9] There was also an attempt to use the hypothesis to explain large nuclear genomes of salamander, but researchers found opposite results than expected, including lower long-term strength of genetic drift.[10]

  1. ^ a b c d Lynch, Michael; Conery, John S. (2003-11-21). "The Origins of Genome Complexity". Science. 302 (5649): 1401–1404. doi:10.1126/science.1089370. ISSN 0036-8075.
  2. ^ a b Lynch, Michael; Bobay, Louis-Marie; Catania, Francesco; Gout, Jean-François; Rho, Mina (2011-09-22). "The Repatterning of Eukaryotic Genomes by Random Genetic Drift". Annual Review of Genomics and Human Genetics. 12 (1): 347–366. doi:10.1146/annurev-genom-082410-101412. ISSN 1527-8204. PMC 4519033. PMID 21756106.{{cite journal}}: CS1 maint: PMC format (link)
  3. ^ a b Lynch, M. (2006-03-24). "Mutation Pressure and the Evolution of Organelle Genomic Architecture". Science. 311 (5768): 1727–1730. doi:10.1126/science.1118884. ISSN 0036-8075.
  4. ^ a b c Lynch, Michael (2006-02-01). "The Origins of Eukaryotic Gene Structure". Molecular Biology and Evolution. 23 (2): 450–468. doi:10.1093/molbev/msj050. ISSN 0737-4038.
  5. ^ Lynch, Michael (2006-10-13). "Streamlining and Simplification of Microbial Genome Architecture". Annual Review of Microbiology. 60 (1): 327–349. doi:10.1146/annurev.micro.60.080805.142300. ISSN 0066-4227.
  6. ^ Smith, D. R.; Lee, R. W. (2010-10-01). "Low Nucleotide Diversity for the Expanded Organelle and Nuclear Genomes of Volvox carteri Supports the Mutational-Hazard Hypothesis". Molecular Biology and Evolution. 27 (10): 2244–2256. doi:10.1093/molbev/msq110. ISSN 0737-4038.
  7. ^ Gaouda, Hager; Hamaji, Takashi; Yamamoto, Kayoko; Kawai-Toyooka, Hiroko; Suzuki, Masahiro; Noguchi, Hideki; Minakuchi, Yohei; Toyoda, Atsushi; Fujiyama, Asao; Nozaki, Hisayoshi; Smith, David Roy (2018-09-01). Chaw, Shu-Miaw (ed.). "Exploring the Limits and Causes of Plastid Genome Expansion in Volvocine Green Algae". Genome Biology and Evolution. 10 (9): 2248–2254. doi:10.1093/gbe/evy175. ISSN 1759-6653. PMC 6128376. PMID 30102347.{{cite journal}}: CS1 maint: PMC format (link)
  8. ^ Yang, Yu-Fei; Zhu, Tao; Niu, Deng-Ke (2013-04-XX). "Association of Intron Loss with High Mutation Rate in Arabidopsis: Implications for Genome Size Evolution". Genome Biology and Evolution. 5 (4): 723–733. doi:10.1093/gbe/evt043. ISSN 1759-6653. PMC 4104619. PMID 23516254. {{cite journal}}: Check date values in: |date= (help)CS1 maint: PMC format (link)
  9. ^ Sloan, Daniel B.; Alverson, Andrew J.; Chuckalovcak, John P.; Wu, Martin; McCauley, David E.; Palmer, Jeffrey D.; Taylor, Douglas R. (2012-01-17). Gray, Michael William (ed.). "Rapid Evolution of Enormous, Multichromosomal Genomes in Flowering Plant Mitochondria with Exceptionally High Mutation Rates". PLoS Biology. 10 (1): e1001241. doi:10.1371/journal.pbio.1001241. ISSN 1545-7885. PMC 3260318. PMID 22272183.{{cite journal}}: CS1 maint: PMC format (link) CS1 maint: unflagged free DOI (link)
  10. ^ Mohlhenrich, Erik Roger; Lockridge Mueller, Rachel (September 27, 2016). "Genetic drift and mutational hazard in the evolution of salamander genomic gigantism". Evolution. 70: 2865–2878 – via JSTOR.
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