Yokoyama Akihiko, Wang Zhong, Wysocka Joanna, Sanyal Mrinmoy, Aufiero Deborah J, Kitabayashi Issay, Herr Winship, Cleary Michael L
Department of Pathology, Stanford University School of Medicine, Stanford, CA 94305, USA.
Mol Cell Biol. 2004 Jul;24(13):5639-49. doi: 10.1128/MCB.24.13.5639-5649.2004.
MLL (for mixed-lineage leukemia) is a proto-oncogene that is mutated in a variety of human leukemias. Its product, a homolog of Drosophila melanogaster trithorax, displays intrinsic histone methyltransferase activity and functions genetically to maintain embryonic Hox gene expression. Here we report the biochemical purification of MLL and demonstrate that it associates with a cohort of proteins shared with the yeast and human SET1 histone methyltransferase complexes, including a homolog of Ash2, another Trx-G group protein. Two other members of the novel MLL complex identified here are host cell factor 1 (HCF-1), a transcriptional coregulator, and the related HCF-2, both of which specifically interact with a conserved binding motif in the MLL(N) (p300) subunit of MLL and provide a potential mechanism for regulating its antagonistic transcriptional properties. Menin, a product of the MEN1 tumor suppressor gene, is also a component of the 1-MDa MLL complex. Abrogation of menin expression phenocopies loss of MLL and reveals a critical role for menin in the maintenance of Hox gene expression. Oncogenic mutant forms of MLL retain an ability to interact with menin but not other identified complex components. These studies link the menin tumor suppressor protein with the MLL histone methyltransferase machinery, with implications for Hox gene expression in development and leukemia pathogenesis.
MLL(混合谱系白血病)是一种原癌基因,在多种人类白血病中发生突变。其产物是果蝇三胸节蛋白的同源物,具有内在的组蛋白甲基转移酶活性,在遗传上发挥作用以维持胚胎Hox基因的表达。在此,我们报告了MLL的生化纯化,并证明它与酵母和人类SET1组蛋白甲基转移酶复合物共有的一组蛋白质相关联,包括Ash2的同源物,另一种Trx-G组蛋白。本文鉴定的新型MLL复合物的另外两个成员是宿主细胞因子1(HCF-1),一种转录共调节因子,以及相关的HCF-2,它们都与MLL的MLL(N)(p300)亚基中的保守结合基序特异性相互作用,并提供了一种调节其拮抗转录特性的潜在机制。Menin是MEN1肿瘤抑制基因的产物,也是1-MDa MLL复合物的一个组成部分。Menin表达的缺失模拟了MLL的缺失,并揭示了menin在维持Hox基因表达中的关键作用。致癌性MLL突变体形式保留了与menin相互作用的能力,但不能与其他已鉴定的复合物成分相互作用。这些研究将menin肿瘤抑制蛋白与MLL组蛋白甲基转移酶机制联系起来,对发育过程中的Hox基因表达和白血病发病机制具有重要意义。