ZRF1 Chromatin Regulators Have Polycomb Silencing and Independent Roles in Development

ZRF1 染色质调节因子具有多梳沉默作用,并在发育中发挥独立作用

阅读:6
作者:Jing Feng, Donghong Chen, Alexandre Berr, Wen-Hui Shen

Abstract

Histone H2A monoubiquitination (H2Aub1), catalyzed by Polycomb-Repressive Complex1 (PRC1), is a key epigenetic mark in Polycomb silencing. However, little is known about how H2Aub1 is read to exert downstream physiological functions. The animal ZUOTIN-RELATED FACTOR1 (ZRF1) has been reported to bind H2Aub1 to promote or repress the expression of varied target genes. Here, we show that the Arabidopsis (Arabidopsis thaliana) ZRF1 homologs, AtZRF1a and AtZRF1b, are key regulators of multiple processes during plant growth and development. Loss of function of both AtZRF1a and AtZRF1b in atzrf1a atzrf1b mutants causes seed germination delay, small plant size, abnormal meristem activity, abnormal flower development, as well as gametophyte transmission and embryogenesis defects. Some of these defects overlap with those described previously in the PRC1-defective mutants atbmi1a atbmi1b and atring1a atring1b, but others are specific to atzrf1a atzrf1b In line with this, 4,519 genes (representing more than 14% of all genes) within the Arabidopsis genome are found differentially expressed in atzrf1a atzrf1b seedlings, and among them, 114 genes are commonly up-regulated in atring1a atring1b and atbmi1a atbmi1b Finally, we show that in both atzrf1a atzrf1b and atbmi1a atbmi1b seedlings, the seed developmental genes ABSCISIC ACID INSENSITIVE3, CRUCIFERIN3, and CHOTTO1 are derepressed, in association with the reduced levels of H2Aub1 and histone H3 lysine-27 trimethylation (H3K27me3). Collectively, our results indicate that AtZRF1a/b play both PRC1-related and PRC1-unrelated functions in regulating plant growth and development and that AtZRF1a/b promote H2Aub1 and H3K27me3 deposition in gene suppression. Our work provides novel insight into the mechanisms of function of this family of evolutionarily conserved chromatin regulators.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。