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An epigenetic basis of inbreeding depression in maize
Inbreeding depression is widespread across plant and animal kingdoms and may arise from the exposure of deleterious alleles and/or loss of overdominant alleles resulting from increased homozygosity, but these genetic models cannot fully explain the phenomenon. Here, we report epigenetic links to inb...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
American Association for the Advancement of Science
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8397266/ https://www.ncbi.nlm.nih.gov/pubmed/34452913 http://dx.doi.org/10.1126/sciadv.abg5442 |
Sumario: | Inbreeding depression is widespread across plant and animal kingdoms and may arise from the exposure of deleterious alleles and/or loss of overdominant alleles resulting from increased homozygosity, but these genetic models cannot fully explain the phenomenon. Here, we report epigenetic links to inbreeding depression in maize. Teosinte branched1/cycloidea/proliferating cell factor (TCP) transcription factors control plant development. During successive inbreeding among inbred lines, thousands of genomic regions across TCP-binding sites (TBS) are hypermethylated through the H3K9me2-mediated pathway. These hypermethylated regions are accompanied by decreased chromatin accessibility, increased levels of the repressive histone marks H3K27me2 and H3K27me3, and reduced binding affinity of maize TCP-proteins to TBS. Consequently, hundreds of TCP-target genes involved in mitochondrion, chloroplast, and ribosome functions are down-regulated, leading to reduced growth vigor. Conversely, random mating can reverse corresponding hypermethylation sites and TCP-target gene expression, restoring growth vigor. These results support a unique role of reversible epigenetic modifications in inbreeding depression. |
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