Gene Expression Dominance in Allopolyploids: Hypotheses and Models
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作者:
Bottani, Samuel
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UMR 7057, Mat & Syst Complexes, F-75013 Paris, France
Univ Paris Diderot Paris VII, F-75205 Paris 13, FranceUMR 7057, Mat & Syst Complexes, F-75013 Paris, France
Bottani, Samuel
[1
,2
]
Zabet, Nicolae Radu
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Univ Essex, Sch Biol Sci, Colchester CO4 3SQ, Essex, EnglandUMR 7057, Mat & Syst Complexes, F-75013 Paris, France
Zabet, Nicolae Radu
[3
]
Wendel, Jonathan F.
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Iowa State Univ, Dept Ecol Evolut & Organismal Biol, Ames, IA 50011 USAUMR 7057, Mat & Syst Complexes, F-75013 Paris, France
Wendel, Jonathan F.
[4
]
Veitia, Reiner A.
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Univ Paris Diderot Paris VII, F-75205 Paris 13, France
Univ Paris Diderot, Inst Jacques Monod, CNRS UMR7592, F-75013 Paris, FranceUMR 7057, Mat & Syst Complexes, F-75013 Paris, France
Veitia, Reiner A.
[2
,5
]
机构:
[1] UMR 7057, Mat & Syst Complexes, F-75013 Paris, France
[2] Univ Paris Diderot Paris VII, F-75205 Paris 13, France
The classical example of nonadditive contributions of the two parents to allopolyploids is nucleolar dominance, which entails silencing of one parental set of ribosomal RNA genes. This has been observed for many other loci. The prevailing explanation for this genome-wide expression disparity is that the two merged genomes differ in their transposable element (TE) complement and in their level of TE-mediated repression of gene expression. Alternatively, and not exclusively, gene expression dominance may arise from mismatches between trans effectors and their targets. Here, we explore quantitative models of regulatory mismatches leading to gene expression dominance. We also suggest that, when pairs of merged genomes are similar from one allopolyploidization event to another, gene-level and genome dominance patterns should also be similar.