Minina Elena A, Reza Salim Hossain, Gutierrez-Beltran Emilio, Elander Pernilla H, Bozhkov Peter V, Moschou Panagiotis N
Department of Molecular Sciences, Uppsala BioCenter, Swedish University of Agricultural Sciences and Linnean Center for Plant Biology, PO Box 7015, Uppsala SE-75007, Sweden
Department of Molecular Sciences, Uppsala BioCenter, Swedish University of Agricultural Sciences and Linnean Center for Plant Biology, PO Box 7015, Uppsala SE-75007, Sweden.
J Cell Sci. 2017 Mar 15;130(6):1051-1063. doi: 10.1242/jcs.196865. Epub 2017 Jan 30.
Factors regulating dynamics of chromatin structure have direct impact on expression of genetic information. Cohesin is a multi-subunit protein complex that is crucial for pairing sister chromatids during cell division, DNA repair and regulation of gene transcription and silencing. In non-plant species, cohesin is loaded on chromatin by the Scc2-Scc4 complex (also known as the NIBPL-MAU2 complex). Here, we identify the homolog of Scc4, which we denote (At)SCC4, and show that it forms a functional complex with AtSCC2, the homolog of Scc2. We demonstrate that AtSCC2 and AtSCC4 act in the same pathway, and that both proteins are indispensable for cell fate determination during early stages of embryo development. Mutant embryos lacking either of these proteins develop only up to the globular stage, and show the suspensor overproliferation phenotype preceded by ectopic auxin maxima distribution. We further establish a new assay to reveal the AtSCC4-dependent dynamics of cohesin loading on chromatin Our findings define the Scc2-Scc4 complex as an evolutionary conserved machinery controlling cohesin loading and chromatin structure maintenance, and provide new insight into the plant-specific role of this complex in controlling cell fate during embryogenesis.
调节染色质结构动态变化的因素对遗传信息的表达有直接影响。黏连蛋白是一种多亚基蛋白复合体,在细胞分裂过程中对姐妹染色单体配对、DNA修复以及基因转录和沉默的调控起着关键作用。在非植物物种中,黏连蛋白由Scc2 - Scc4复合体(也称为NIBPL - MAU2复合体)加载到染色质上。在此,我们鉴定出Scc4的同源物,将其命名为(At)SCC4,并表明它与Scc2的同源物AtSCC2形成功能复合体。我们证明AtSCC2和AtSCC4在同一途径中起作用,并且这两种蛋白在胚胎发育早期的细胞命运决定中都是不可或缺的。缺乏这两种蛋白中任何一种的突变胚胎只能发育到球形期,并表现出胚柄过度增殖的表型,其之前伴随着生长素异位最大值分布。我们进一步建立了一种新方法来揭示AtSCC4依赖的黏连蛋白加载到染色质上的动态变化。我们的研究结果将Scc2 - Scc4复合体定义为一种进化上保守的机制,用于控制黏连蛋白加载和染色质结构维持,并为该复合体在胚胎发生过程中控制细胞命运的植物特异性作用提供了新的见解。