Fun30 核小体重塑因子调节. 的白- opaque 转换。
Fun30 nucleosome remodeller regulates white-to-opaque switching in .
机构信息
State Key Laboratory of Molecular Biology, Shanghai Institute of Biochemistry and Cell Biology, Center for Excellence in Molecular Cell Science, Chinese Academy of Sciences, Shanghai 200031, China.
Key Laboratory of Pathogenic Fungi and Mycotoxins of Fujian Province, School of Life Sciences, Fujian Agriculture and Forestry University, Fuzhou 350002, China.
出版信息
Acta Biochim Biophys Sin (Shanghai). 2023 Mar 25;55(3):508-517. doi: 10.3724/abbs.2023031.
( . ) is an opportunistic pathogen in humans and possesses a white-opaque heritable switching system. Wor1 is a master regulator of white-opaque switching and is essential for opaque cell formation in . . However, the regulatory network of Wor1 in white-opaque switching is still vague. In this study, we obtain a series of Wor1-interacting proteins using LexA-Wor1 as bait. Among these proteins, function unknown now 30 (Fun30) interacts with Wor1 and . Fun30 expression is upregulated in opaque cells at the transcriptional and protein levels. Loss of attenuates white-to-opaque switching, while ectopic expression of significantly increases white-to-opaque switching in an ATPase activity-dependent manner. Furthermore, upregulation is dependent on CO ; loss of , a key CO -sensing transcriptional regulator, abolishes upregulation. Interestingly, deletion of affects the expression regulation feedback loop. Thus, our results indicate that the chromatin remodeller Fun30 interacts with Wor1 and is required for expression and opaque cell formation.
（. ）是人类中的机会性病原体，具有白色-不透明遗传开关系统。 Wor1 是白色-不透明开关的主要调节剂，对于. . 中不透明细胞的形成是必不可少的。然而，Wor1 在白色-不透明开关中的调控网络仍然不清楚。在这项研究中，我们使用 LexA-Wor1 作为诱饵获得了一系列 Wor1 相互作用蛋白。在这些蛋白中，功能未知现在 30 （Fun30）与 Wor1 和 相互作用。Fun30 的表达在转录和蛋白质水平上在不透明细胞中上调。 的缺失削弱了白色到不透明的转换，而 的异位表达以 ATPase 活性依赖性方式显著增加了白色到不透明的转换。此外， 的上调依赖于 CO ；关键的 CO 感应转录调节剂 的缺失，消除了 的上调。有趣的是， 的缺失会影响 的表达调控反馈回路。因此，我们的结果表明，染色质重塑酶 Fun30 与 Wor1 相互作用，是 的表达和不透明细胞形成所必需的。
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