Department of Molecular Genetics, Weizmann Institute of Science, Rehovot P.O. Box 26, Israel.
Cells. 2024 Oct 9;13(19):1670. doi: 10.3390/cells13191670.
A group of intrinsically disordered proteins (IDPs) are subject to 20S proteasomal degradation in a ubiquitin-independent manner. Recently, we have reported that many IDPs/IDRs are targeted to the 20S proteasome via interaction with the C-terminus of the PSMA3 subunit, termed the PSMA3 Trapper. In this study, we investigated the biological significance of the IDP-Trapper interaction using the IDP p21. Using a split luciferase reporter assay and conducting detailed p21 mutagenesis, we first identified the p21 RRLIF box, localized at the C-terminus, as mediating the Trapper interaction in cells. To demonstrate the role of this box in p21 degradation, we edited the genome of HEK293 and HeLa cell lines using a CRISPR strategy. We found that the p21 half-life increased in cells with either a deleted or mutated p21 RRLIF box. The edited cell lines displayed an aberrant cell cycle pattern under normal conditions and in response to DNA damage. Remarkably, these cells highly expressed senescence hallmark genes in response to DNA damage, highlighting that the increased p21 half-life, not its actual level, regulates senescence. Our findings suggest that the p21 RRLIF box, which mediates interactions with the PSMA3 Trapper, acts as a ubiquitin-independent degron. This degron is positioned adjacent to the previously identified ubiquitin-dependent degron, forming a dual degron module that functionally regulates p21 degradation and its physiological outcomes.
一组无序蛋白(IDP)在非泛素依赖的方式下被 20S 蛋白酶体降解。最近,我们报道称许多 IDP/IDR 通过与 PSMA3 亚基的 C 末端相互作用被靶向到 20S 蛋白酶体,称为 PSMA3 Trapper。在这项研究中,我们使用 IDP p21 研究了 IDP-Trapper 相互作用的生物学意义。使用分裂荧光素酶报告基因测定,并进行详细的 p21 突变分析,我们首先确定了位于 C 末端的 p21 RRLIF 盒介导细胞中的 Trapper 相互作用。为了证明该盒在 p21 降解中的作用,我们使用 CRISPR 策略编辑了 HEK293 和 HeLa 细胞系的基因组。我们发现,具有删除或突变的 p21 RRLIF 盒的细胞中 p21 的半衰期增加。在正常条件下和响应 DNA 损伤时,编辑后的细胞系显示出异常的细胞周期模式。值得注意的是,这些细胞在响应 DNA 损伤时高度表达衰老标志性基因,这表明增加的 p21 半衰期而不是其实际水平调节衰老。我们的研究结果表明,介导与 PSMA3 Trapper 相互作用的 p21 RRLIF 盒充当非泛素依赖性降解基序。该降解基序位于先前鉴定的泛素依赖性降解基序附近,形成一个双降解基序模块,可对 p21 降解及其生理结果进行功能调节。