日本千葉大學(xué)教授巖間厚志率領(lǐng)的研究小組在最新一期美國(guó)《細(xì)胞－干細(xì)胞》雜志上發(fā)表論文說(shuō),，他們發(fā)現(xiàn)，缺失基因“Bmi1”會(huì)影響造血干細(xì)胞生成血液細(xì)胞,。
研究人員對(duì)實(shí)驗(yàn)鼠進(jìn)行基因操作,，使其失去基因“Bmi1”。結(jié)果實(shí)驗(yàn)鼠本來(lái)應(yīng)該生成紅細(xì)胞或白細(xì)胞的造血干細(xì)胞,，只生成了特定的淋巴細(xì)胞,。
研究人員認(rèn)為，沒(méi)有“Bmi1”基因,，造血干細(xì)胞中平時(shí)不發(fā)生作用的其他基因開(kāi)始發(fā)揮作用,，導(dǎo)致造血干細(xì)胞失去多功能性，只生成了淋巴細(xì)胞。他們由此判斷,，“Bmi1”對(duì)于造血干細(xì)胞分化成各種血液細(xì)胞是必不可少的,。（生物谷Bioon.com）
2010年干細(xì)胞技術(shù)與應(yīng)用講座即將于上海召開(kāi)，詳情查看：http://www.stemcellasia.net/
生物谷推薦原始出處：
Cell Stem Cell, Volume 6, Issue 3, 279-286, 5 March 2010 10.1016/j.stem.2010.01.005
Poised Lineage Specification in Multipotential Hematopoietic Stem and Progenitor Cells by the Polycomb Protein Bmi1
Hideyuki Oguro, Jin Yuan, Hitoshi Ichikawa, Tomokatsu Ikawa, Satoshi Yamazaki, Hiroshi Kawamoto, Hiromitsu Nakauchi, Atsushi Iwama
Department of Cellular and Molecular Medicine, Graduate School of Medicine, Chiba University, Chiba 260-8670, Japan JST, CREST, Sanbancho, Chiyoda-ku, Tokyo 102-0075, Japan JST, ERATO, Sanbancho, Chiyoda-ku, Tokyo 102-0075, Japan Genetics Division, National Cancer Center Research Institute, Tokyo, 104-0045, Japan Laboratory for Lymphocyte Development, RIKEN Research Center for Allergy and Immunology, Yokohama 230-0045, Japan Laboratory of Stem Cell Therapy, Center for Experimental Medicine, Institute of Medical Sciences, University of Tokyo, Tokyo 108-8679, Japan Corresponding author
Polycomb group (PcG) proteins are essential regulators of stem cells. PcG and trithorax group proteins mark developmental regulator gene promoters with bivalent domains consisting of overlapping repressive and activating histone modifications to keep them poised for activation in embryonic stem cells. Bmi1, a component of PcG complexes, maintains the self-renewal capacity of adult stem cells, but its role in multipotency remains obscure. Here we show that Bmi1 is critical for multipotency of hematopoietic stem cells (HSCs) and multipotent progenitors (MPPs). B cell lineage developmental regulator genes, Ebf1 and Pax5, appeared to be transcriptionally repressed by bivalent domains before lineage commitment. Loss of Bmi1 resulted in a resolution of bivalent domains at the Ebf1 and Pax5 loci, leading to their premature expression in HSC/MPPs accompanied by accelerated lymphoid specification and a marked reduction in HSC/MPPs. Thus, Bmi1 is required to reinforce bivalent domains at key developmental regulator gene loci to maintain lineage specification poised for activation in adult stem cells.
