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学界至今仍不断研究根治癌症方法，年仅27岁的香港小子梁子宇，透过老鼠胚胎干细胞和基因研究，首次发现将癌症连根拔起的曙光。他发现，透过控制一种名为ESET的蛋白，便可将致癌干细胞歼灭而不影响正常细胞，是启发根治癌症的新突破。报告已于4月8日出版的国际权威科学期刊《自然》(Nature)上发表。- D6 L4 U" R* B
% d3 o- x; E4 t& C5 ?据香港明报报道，本身也从事基因研究的香港大学校长徐立之对此研究也感可喜，并指香港极需此类优秀人才回流。
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梁子宇的父亲是香港执业西医，但他并无继承父业读医，而是自创新天地。他13岁随家人移居加拿大，在当地完成中学课程后，先后考入英国伦敦大学学院 (UCL)和伦敦帝国学院(IC)学士及硕士毕业，一直钻研香港较冷门的基因研究，专注“表观基因学”。3年前他返回加拿大在英属哥伦比亚大学(UBC)攻读博士课程至今。
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% Z/ F$ F( Z5 ~3 @1 u他透过长途电话接受访问时说，“香港的确是少人研究此学科，但正因为少，就应该去做。”梁子宇拥有一颗赤子心，希望透过所学知识，研究出治疗疾病的新突破，造福病人。+ J1 r! P9 F Y" ~0 @1 R8 ~
, ]+ \; s! _" L0 r8 X“现时治疗癌症的传统方法，是将肿瘤切除，然后做化疗、电疗等，但化疗和电疗除会将癌细胞杀死，就连一些正常的细胞也被杀死；我们的发现可针对致癌的干细胞，做到清除癌细胞但不影响正常细胞。”他与日本京都大学一名也是30出头的研究员松井稔幸研究以往较少人关注的蛋白“ESET”，找到根治癌症的曙光。( e; C+ {$ i: T+ N
1 z3 O0 B3 y- {. U; }8 P' y6 Q E9 Y年纪轻轻便在国际科学舞台露光芒，被问及是否已有香港的大学向他招手，梁子宇说，确有香港的大学教授找他，但他指自己仍未博士毕业，回流加盟是言之尚早。
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梁子宇“放洋”多年，但家在香港，每年放假也会回港，对这片土地很有归属感。他立下决心，学成后一定回来作贡献，但不会是短期内的事。“我想在国外从事研究一段时间，希望有一番成绩后，才返香港领导研究队伍从事研究。”
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港大校长徐立之表示，香港年轻人能在科研上有成就并获国际认同，值得恭喜，港大当然有兴趣汲纳世界各地不同年龄和学科的优秀人才，而香港本身也有很多优秀的科学家。（生物谷Bioon.com)# z$ j0 B- H0 z' {- S
6 n0 {" Y' }8 W4 T1 N0 EProviral silencing in embryonic stem cells requires the histone methyltransferase ESET8 j6 w) N9 s+ ^/ h
Toshiyuki Matsui1,2,5, Danny Leung3,5, Hiroki Miyashita1,2, Irina A. Maksakova3, Hitoshi Miyachi1, Hiroshi Kimura4, Makoto Tachibana1,2, Matthew C. Lorincz3 & Yoichi Shinkai1,27 l5 i4 I1 }! M! p. n0 y* @
. Y' L4 O+ U3 {/ g- O- k1Experimental Research Center for Infectious Diseases, Institute for Virus Research, and,
$ C) b7 S- A9 M; z9 L W* x2Graduate School of Biostudies, Kyoto University, 53 Shogoin, Kawara-cho, Sakyo-ku, Kyoto 606-8507, Japan
* C3 p- C3 ~+ F3Department of Medical Genetics, Life Sciences Institute, The University of British Columbia, Vancouver, British Columbia V6T 1Z3, Canada
' b( c% u7 j+ X4Graduate School of Frontier Biosciences, Osaka University, Suita, Osaka 565-0871, Japan' z& y* |. _$ O
5These authors contributed equally to this work.
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& W( l! i- B+ W& V$ QEndogenous retroviruses (ERVs), retrovirus-like elements with long terminal repeats, are widely dispersed in the euchromatic compartment in mammalian cells, comprising ~10% of the mouse genome1. These parasitic elements are responsible for >10% of spontaneous mutations2. Whereas DNA methylation has an important role in proviral silencing in somatic and germ-lineage cells3, 4, 5, an additional DNA-methylation-independent pathway also functions in embryonal carcinoma and embryonic stem (ES) cells to inhibit transcription of the exogenous gammaretrovirus murine leukaemia virus (MLV)6, 7, 8. Notably, a recent genome-wide study revealed that ERVs are also marked by histone H3 lysine 9 trimethylation (H3K9me3) and H4K20me3 in ES cells but not in mouse embryonic fibroblasts9. However, the role that these marks have in proviral silencing remains unexplored. Here we show that the H3K9 methyltransferase ESET (also called SETDB1 or KMT1E) and the Krüppel-associated box (KRAB)-associated protein 1 (KAP1, also called TRIM28)10, 11 are required for H3K9me3 and silencing of endogenous and introduced retroviruses specifically in mouse ES cells. Furthermore, whereas ESET enzymatic activity is crucial for HP1 binding and efficient proviral silencing, the H4K20 methyltransferases Suv420h1 and Suv420h2 are dispensable for silencing. Notably, in DNA methyltransferase triple knockout (Dnmt1-/-Dnmt3a-/-Dnmt3b-/-) mouse ES cells, ESET and KAP1 binding and ESET-mediated H3K9me3 are maintained and ERVs are minimally derepressed. We propose that a DNA-methylation-independent pathway involving KAP1 and ESET/ESET-mediated H3K9me3 is required for proviral silencing during the period early in embryogenesis when DNA methylation is dynamically reprogrammed
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发表于 2010-12-17 21:13
发表于 2011-4-22 18:17
