A small UTX stabilization domain of Trr is conserved within mammalian MLL3-4/COMPASS and is sufficient to rescue loss of viability in null animals.

A small UTX stabilization domain of Trr is conserved within mammalian MLL3-4/COMPASS and is sufficient to rescue loss of viability in null animals.
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DOI:
10.1101/gad.339762.120
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发表时间:
2020-11-01
影响因子:
10.5
通讯作者:
Shilatifard A
Shilatifard A
中科院分区:
生物学1区
文献类型:
--
作者:
Rickels R;Wang L;Iwanaszko M;Ozark PA;Morgan MA;Piunti A;Khalatyan N;Soliman SHA;Rendleman EJ;Savas JN;Smith ER;Shilatifard A

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在这项研究中,Rickel 等人。鉴定了 Trr 的基本组蛋白甲基转移酶独立功能,使用筛选鉴定了足以挽救 Trr 无效致死性的最小 Trr 结构域,并证明该结构域在体内结合并稳定 Utx。他们的研究结果表明,COMPASS 依赖性 UTX 稳定是 Trr/MLL3/MLL4 的重要非催化功能,这表明稳定 UTX 可能是具有 MLL3/4 功能丧失突变的癌症的治疗策略。与这些 COMPASS 成员的全基因缺失相比,果蝇增强子 H3K4 单甲基转移酶 Trr 及其哺乳动物同源物 MLL3/4 内的催化失活突变仅导致基因表达的微小变化。为了确定 Trr 的基本的组蛋白甲基转移酶独立功能,我们进行了筛选,以确定足以挽救 Trr 无效致死性的最小 Trr 结构域,并证明该结构域在体内结合并稳定 Utx。使用同源 MLL3/MLL4 人类序列,我们绘制了一个短的~80 个氨基酸的 UTX 稳定结​​构域 (USD),该结构域在没有 MLL3/4 其余部分的情况下促进 UTX 稳定性。当 USD 与 MLL4 HMG-box 融合时,核 UTX 稳定性得到增强。因此,COMPASS 依赖性 UTX 稳定是 Trr/MLL3/MLL4 的重要非催化功能,这表明稳定 UTX 可能是具有 MLL3/4 功能丧失突变的癌症的治疗策略。
In this study, Rickel et al. identified essential histone methylatransferase-independent functions of Trr, used a screen to identify a minimal Trr domain sufficient to rescue Trr-null lethality, and demonstrated that this domain binds and stabilizes Utx in vivo. Their findings show that COMPASS-dependent UTX stabilization is an essential noncatalytic function of Trr/MLL3/MLL4, suggesting that stabilizing UTX could be a therapeutic strategy for cancers with MLL3/4 loss-of-function mutations. Catalytic-inactivating mutations within the Drosophila enhancer H3K4 mono-methyltransferase Trr and its mammalian homologs, MLL3/4, cause only minor changes in gene expression compared with whole-gene deletions for these COMPASS members. To identify essential histone methyltransferase-independent functions of Trr, we screened to identify a minimal Trr domain sufficient to rescue Trr-null lethality and demonstrate that this domain binds and stabilizes Utx in vivo. Using the homologous MLL3/MLL4 human sequences, we mapped a short ∼80-amino-acid UTX stabilization domain (USD) that promotes UTX stability in the absence of the rest of MLL3/4. Nuclear UTX stability is enhanced when the USD is fused with the MLL4 HMG-box. Thus, COMPASS-dependent UTX stabilization is an essential noncatalytic function of Trr/MLL3/MLL4, suggesting that stabilizing UTX could be a therapeutic strategy for cancers with MLL3/4 loss-of-function mutations.
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