Histone H3.3 and cancer: A potential reader connection

被引：19

作者：

Lan, Fei ^{[1
,2
,3
]}

Shi, Yang ^{[4
,5
]}

机构：

[1] Fudan Univ, Sch Basic Med, Shanghai Med Coll, Key Lab Epigenet,Shanghai Minist Educ, Shanghai 200032, Peoples R China

[2] Fudan Univ, Inst Biomed Sci, Shanghai Med Coll, Shanghai 200032, Peoples R China

[3] Fudan Univ, Childrens Hosp, Key Lab Birth Defect, Shanghai 201102, Peoples R China

[4] Harvard Univ, Sch Med, Dept Cell Biol, Boston, MA 02115 USA

[5] Boston Childrens Hosp, Div Newborn Med, Boston, MA 02115 USA

来源：

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA | 2015年 / 112卷 / 22期

关键词：

histone; H3.3; H3.3K36me3; cancer; BS69; RNA-POLYMERASE-II; ADENOVIRUS E1A-ASSOCIATED PROTEIN; ACTIVATING ACVR1 MUTATIONS; INTRINSIC PONTINE GLIOMA; LYSINE; 36; TRIMETHYLATION; HIGH-GRADE GLIOMAS; VARIANT H3.3; PWWP DOMAIN; PEDIATRIC GLIOBLASTOMA; INTRON RETENTION;

D O I：

10.1073/pnas.1418996111

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

The building block of chromatin is nucleosome, which consists of 146 base pairs of DNA wrapped around a histone octamer composed of two copies of histone H2A, H2B, H3, and H4. Significantly, the somatic missense mutations of the histone H3 variant, H3.3, are associated with childhood and young-adult tumors, such as pediatric high-grade astrocytomas, as well as chondroblastoma and giant-cell tumors of the bone. The mechanisms by which these histone mutations cause cancer are by and large unclear. Interestingly, two recent studies identified BS69/ZMYND11, which was proposed to be a candidate tumor suppressor, as a specific reader for a modified form of H3.3 (H3.3K36me3). Importantly, some H3.3 cancer mutations are predicted to abrogate the H3.3K36me3/BS69 interaction, suggesting that this interaction may play an important role in tumor suppression. These new findings also raise the question of whether H3.3 cancer mutations may lead to the disruption and/or gain of interactions of additional cellular factors that contribute to tumorigenesis.

引用

页码：6814 / 6819

页数：6

共 66 条

[1] The histone variant H3.3 marks active chromatin by replication-independent nucleosome assembly [J].

Ahmad, K ;

Henikoff, S .

MOLECULAR CELL, 2002, 9 (06) :1191-1200

[2] H3F3A K27M mutations in thalamic gliomas from young adult patients [J].

Aihara, Koki ;

Mukasa, Akitake ;

Gotoh, Kengo ;

Saito, Kuniaki ;

Nagae, Genta ;

Tsuji, Shingo ;

Tatsuno, Kenji ;

Yamamoto, Shogo ;

Takayanagi, Shunsaku ;

Narita, Yoshitaka ;

Shibui, Soichiro ;

Aburatani, Hiroyuki ;

Saito, Nobuhito .

NEURO-ONCOLOGY, 2014, 16 (01) :140-146

[3] The ribosomal translocase homologue Snu114p is involved in unwinding U4/U6 RNA during activation of the spliceosome [J].

Bartels, C ;

Klatt, C ;

Lührmann, R ;

Fabrizio, P .

EMBO REPORTS, 2002, 3 (09) :875-880

[4] The human SWI/SNF subunit Brm is a regulator of alternative splicing [J].

Batsché, E ;

Yaniv, M ;

Muchardt, C .

NATURE STRUCTURAL & MOLECULAR BIOLOGY, 2006, 13 (01) :22-29

[5] Distinct H3F3A and H3F3B driver mutations define chondroblastoma and giant cell tumor of bone [J].

Behjati, Sam ;

Tarpey, Patrick S. ;

Presneau, Nadege ;

Scheipl, Susanne ;

Pillay, Nischalan ;

Van Loo, Peter ;

Wedge, David C. ;

Cooke, Susanna L. ;

Gundem, Gunes ;

Davies, Helen ;

Nik-Zainal, Serena ;

Martin, Sancha ;

McLaren, Stuart ;

Goodie, Victoria ;

Robinson, Ben ;

Butler, Adam ;

Teague, Jon W. ;

Halai, Dina ;

Khatri, Bhavisha ;

Myklebost, Ola ;

Baumhoer, Daniel ;

Jundt, Gernot ;

Hamoudi, Rifat ;

Tirabosco, Roberto ;

Amary, M. Fernanda ;

Futreal, P. Andrew ;

Stratton, Michael R. ;

Campbell, Peter J. ;

Flanagan, Adrienne M. .

NATURE GENETICS, 2013, 45 (12) :1479-U105

[6] Reduced H3K27me3 and DNA Hypomethylation Are Major Drivers of Gene Expression in K27M Mutant Pediatric High-Grade Gliomas [J].

Bender, Sebastian ;

Tang, Yujie ;

Lindroth, Anders M. ;

Hovestadt, Volker ;

Jones, David T. W. ;

Kool, Marcel ;

Zapatka, Marc ;

Northcott, Paul A. ;

Sturm, Dominik ;

Wang, Wei ;

Radlwimmer, Bernhard ;

Hojfeldt, Jonas W. ;

Truffaux, Nathalene ;

Castel, David ;

Schubert, Simone ;

Ryzhova, Marina ;

Seker-Cin, Huriye ;

Gronych, Jan ;

Johann, Pascal David ;

Stark, Sebastian ;

Meyer, Jochen ;

Milde, Till ;

Schuhmann, Martin ;

Ebinger, Martin ;

Monoranu, Camelia-Maria ;

Ponnuswami, Anitha ;

Chen, Spenser ;

Jones, Chris ;

Witt, Olaf ;

Collins, V. Peter ;

von Deimling, Andreas ;

Jabado, Nada ;

Puget, Stephanie ;

Grill, Jacques ;

Helin, Kristian ;

Korshunov, Andrey ;

Lichter, Peter ;

Monje, Michelle ;

Plass, Christoph ;

Cho, Yoon-Jae ;

Pfister, Stefan M. .

CANCER CELL, 2013, 24 (05) :660-672

[7] A bivalent chromatin structure marks key developmental genes in embryonic stem cells [J].

Bernstein, BE ;

Mikkelsen, TS ;

Xie, XH ;

Kamal, M ;

Huebert, DJ ;

Cuff, J ;

Fry, B ;

Meissner, A ;

Wernig, M ;

Plath, K ;

Jaenisch, R ;

Wagschal, A ;

Feil, R ;

Schreiber, SL ;

Lander, ES .

CELL, 2006, 125 (02) :315-326

[8] Histone H3.3 Mutations Drive Pediatric Glioblastoma through Upregulation of MYCN [J].

Bjerke, Lynn ;

Mackay, Alan ;

Nandhabalan, Meera ;

Burford, Anna ;

Jury, Alexa ;

Popov, Sergey ;

Bax, Dorine A. ;

Carvalho, Diana ;

Taylor, Kathryn R. ;

Vinci, Maria ;

Bajrami, Ilirjana ;

McGonnell, Imelda M. ;

Lord, Christopher J. ;

Reis, Rui M. ;

Hargrave, Darren ;

Ashworth, Alan ;

Workman, Paul ;

Jones, Chris .

CANCER DISCOVERY, 2013, 3 (05) :512-519

[9] Nucleosomes can form a polar barrier to transcript elongation by RNA polymerase II [J].

Bondarenko, Vladimir A. ;

Steele, Louise M. ;

Ujvari, Andrea ;

Gaykalova, Daria A. ;

Kulaeva, Olga I. ;

Polikanov, Yury S. ;

Luse, Donal S. ;

Studitsky, Vasily M. .

MOLECULAR CELL, 2006, 24 (03) :469-479

[10] Widespread intron retention in mammals functionally tunes transcriptomes [J].

Braunschweig, Ulrich ;

Barbosa-Morais, Nuno L. ;

Pan, Qun ;

Nachman, Emil N. ;

Alipanahi, Babak ;

Gonatopoulos-Pournatzis, Thomas ;

Frey, Brendan ;

Irimia, Manuel ;

Blencowe, Benjamin J. .

GENOME RESEARCH, 2014, 24 (11) :1774-1786

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