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异位施加抑制性组蛋白修饰 H3K9me2 可在 中建立合子后生殖隔离。

Ectopic application of the repressive histone modification H3K9me2 establishes post-zygotic reproductive isolation in .

机构信息

Department of Plant Biology, Uppsala BioCenter, Swedish University of Agricultural Sciences, Linnean Center of Plant Biology, Uppsala 75007, Sweden.

Department of Plant Biotechnology and Bioinformatics, Ghent University, Ghent 9052, Belgium.

出版信息

Genes Dev. 2017 Jun 15;31(12):1272-1287. doi: 10.1101/gad.299347.117. Epub 2017 Jul 25.

Abstract

Hybrid seed lethality as a consequence of interspecies or interploidy hybridizations is a major mechanism of reproductive isolation in plants. This mechanism is manifested in the endosperm, a dosage-sensitive tissue supporting embryo growth. Deregulated expression of imprinted genes such as () underpin the interploidy hybridization barrier in ; however, the mechanisms of their action remained unknown. In this study, we show that ADM interacts with the AT hook domain protein AHL10 and the SET domain-containing SU(VAR)3-9 homolog SUVH9 and ectopically recruits the heterochromatic mark H3K9me2 to AT-rich transposable elements (TEs), causing deregulated expression of neighboring genes. Several hybrid incompatibility genes identified in encode for dosage-sensitive heterochromatin-interacting proteins, which has led to the suggestion that hybrid incompatibilities evolve as a consequence of interspecies divergence of selfish DNA elements and their regulation. Our data show that imbalance of dosage-sensitive chromatin regulators underpins the barrier to interploidy hybridization in , suggesting that reproductive isolation as a consequence of epigenetic regulation of TEs is a conserved feature in animals and plants.

摘要

种间或异倍体杂交导致杂种胚败育是植物生殖隔离的主要机制。这种机制表现在胚乳中,胚乳是一种剂量敏感的组织,支持胚胎生长。印迹基因如 () 的表达失调是 异倍体杂交障碍的基础;然而,其作用机制尚不清楚。在这项研究中,我们表明 ADM 与 AT 钩域蛋白 AHL10 和含有 SET 域的 SU(VAR)3-9 同源 SUVH9 相互作用,并异位募集异染色质标记 H3K9me2 到富含 AT 的转座元件 (TEs),导致邻近基因的表达失调。在 中鉴定的几个杂种不亲和基因编码剂量敏感的异染色质相互作用蛋白,这导致了这样的假设,即杂种不亲和性是作为自私 DNA 元件及其调控的种间分歧的结果而进化的。我们的数据表明,剂量敏感染色质调节剂的失衡是 异倍体杂交障碍的基础,这表明转座元件的表观遗传调控导致的生殖隔离是动物和植物的一个保守特征。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e9b/5558928/24f80e341101/1272f01.jpg

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