Unifying framework explaining how parental regulatory divergence can drive gene expression in hybrids and allopolyploids.
Autor: | Janko K; Laboratory of Non-Mendelian Evolution, Institute of Animal Physiology and Genetics of the Czech Aacademy of Sciences, Rumburská 89, 277 21, Liběchov, Czech Republic. k_janko@yahoo.com., Eisner J; Department of Mathematics, Faculty of Science, University of South Bohemia in České Budějovice, Branišovská 1760, 370 05, České Budějovice, Czech Republic.; Department of Biology and Ecology, Faculty of Natural Sciences, University of Ostrava, Chittussiho 10, Ostrava, Czech Republic., Cigler P; Institute of Organic Chemistry and Biochemistry of the CAS, 166 10, Prague, Czech Republic. petr.cigler@uochb.cas.cz., Tichopád T; Department of Biology and Ecology, Faculty of Natural Sciences, University of Ostrava, Chittussiho 10, Ostrava, Czech Republic.; University of South Bohemia in České Budějovice, Faculty of Fisheries and Protection of Waters, South Bohemian Research Center of Aquaculture and Biodiversity of Hydrocenoses, Zátiší 728/II, 389 25, Vodňany, Czech Republic. |
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Jazyk: | angličtina |
Zdroj: | Nature communications [Nat Commun] 2024 Oct 08; Vol. 15 (1), pp. 8714. Date of Electronic Publication: 2024 Oct 08. |
DOI: | 10.1038/s41467-024-52546-5 |
Abstrakt: | Hybridization and polyploidy are powerful evolutionary forces, inducing a range of phenotypic outcomes, including non-additive expression, subgenome dominance, deviations in genomic dosage, and transcriptome downsizing. The reasons for these patterns and whether they are universal adaptive responses to genome merging and doubling remain debated. To address this, we develop a thermodynamic model of gene expression based on transcription factor (TF)-promoter binding. Applied to hybridization between species with divergent gene expression levels, cell volumes, or euchromatic ratios, this model distinguishes the effects of hybridization from those of polyploidy. Our results align with empirical observations, suggesting that gene regulation patterns in hybrids and polyploids often stem from the constrained interplay between inherited diverged regulatory networks rather than from subsequent adaptive evolution. In addition, occurrence of certain phenotypic traits depend on specific assumptions about promoter-TF coevolution and their distribution within the hybrid's nucleoplasm, offering new research avenues to understand the underlying mechanisms. In summary, our model explains how the legacy of divergent species directly influences the phenotypic traits of hybrids and allopolyploids. (© 2024. The Author(s).) |
Databáze: | MEDLINE |
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