HIRA orchestrates a non-canonical dynamic chromatin landscape in senescence and is required for suppression of neoplasia

Taranjit Singh Rai; John C. Cole; David M. Nelson; Dina Dikovskaya; Tony McBryan; William Faller; John v. Tuyn; Nicholas Morrice; Rachael N. Hewitt; Claire Brock; Andrejs Ivanov; Mark E. Drotar; Colin Nixon; William Clark; Owen J. Sansom; Ayala King; Karen Blyth; Peter D. Adams

HIRA orchestrates a non-canonical dynamic chromatin landscape in senescence and is required for suppression of neoplasia

Taranjit Singh Rai, John C. Cole, David M. Nelson, Dina Dikovskaya, Tony McBryan, William Faller, John v. Tuyn, Nicholas Morrice, Rachael N. Hewitt, Claire Brock, Andrejs Ivanov, Mark E. Drotar, Colin Nixon, William Clark, Owen J. Sansom, Ayala King, Karen Blyth, Peter D. Adams

Research output: Contribution to conference › Poster

Abstract

Cellular senescence is a stable proliferation arrest that suppresses tumorigenesis. Cell senescence and associated tumor suppression depend on control of chromatin. Chromatin is dynamically controlled, and its imbalance can promote cancer, as evidenced by recurrent mutations and dysregulation in cancer of H3.3, a histone variant enriched at dynamic chromatin regulatory sites. Hence, it is important to understand the impact of dynamic chromatin control on tumor suppression. We show that non-proliferating tumor suppressive senescent cells express and incorporate histone H3.3 and normally "replication-dependent" histones into a non-canonical, H4K16ac-decorated, dynamic chromatin landscape. A key regulator of this landscape, histone chaperone HIRA, is required for suppression of oncogene-induced neoplasia in vivo. These results indicate a role for a non-canonical, dynamic chromatin landscape in tumor suppression.

Original language	English
Publication status	Published - 9 Sept 2014
Event	Epigenetics & Chromatin CSHL 2014: Cold Spring Harbor Laboratory Meeting on Epigenetics & Chromatin - Cold Spring Harbor Laboratory, Cold Spring Harbor, United States Duration: 9 Sept 2014 → 13 Sept 2014 http://epigenie.com/conferences/epigenetics-chromatin-cshl-2014/ (Notice of meeting)

Conference

Conference	Epigenetics & Chromatin CSHL 2014
Country/Territory	United States
City	Cold Spring Harbor
Period	9/09/14 → 13/09/14
Internet address	http://epigenie.com/conferences/epigenetics-chromatin-cshl-2014/ (Notice of meeting)

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Rai, T. S., Cole, J. C., Nelson, D. M., Dikovskaya, D., McBryan, T., Faller, W., v. Tuyn, J., Morrice, N., Hewitt, R. N., Brock, C., Ivanov, A., Drotar, M. E., Nixon, C., Clark, W., Sansom, O. J., King, A., Blyth, K., & Adams, P. D. (2014). HIRA orchestrates a non-canonical dynamic chromatin landscape in senescence and is required for suppression of neoplasia. Poster session presented at Epigenetics & Chromatin CSHL 2014, Cold Spring Harbor, New York, United States.

@conference{bee183f9deba46de9307d6edf1e398e5,

title = "HIRA orchestrates a non-canonical dynamic chromatin landscape in senescence and is required for suppression of neoplasia",

abstract = "Cellular senescence is a stable proliferation arrest that suppresses tumorigenesis. Cell senescence and associated tumor suppression depend on control of chromatin. Chromatin is dynamically controlled, and its imbalance can promote cancer, as evidenced by recurrent mutations and dysregulation in cancer of H3.3, a histone variant enriched at dynamic chromatin regulatory sites. Hence, it is important to understand the impact of dynamic chromatin control on tumor suppression. We show that non-proliferating tumor suppressive senescent cells express and incorporate histone H3.3 and normally {"}replication-dependent{"} histones into a non-canonical, H4K16ac-decorated, dynamic chromatin landscape. A key regulator of this landscape, histone chaperone HIRA, is required for suppression of oncogene-induced neoplasia in vivo. These results indicate a role for a non-canonical, dynamic chromatin landscape in tumor suppression.",

author = "Rai, {Taranjit Singh} and Cole, {John C.} and Nelson, {David M.} and Dina Dikovskaya and Tony McBryan and William Faller and {v. Tuyn}, John and Nicholas Morrice and Hewitt, {Rachael N.} and Claire Brock and Andrejs Ivanov and Drotar, {Mark E.} and Colin Nixon and William Clark and Sansom, {Owen J.} and Ayala King and Karen Blyth and Adams, {Peter D.}",

year = "2014",

month = sep,

day = "9",

language = "English",

note = "Epigenetics & Chromatin CSHL 2014 : Cold Spring Harbor Laboratory Meeting on Epigenetics & Chromatin ; Conference date: 09-09-2014 Through 13-09-2014",

url = "http://epigenie.com/conferences/epigenetics-chromatin-cshl-2014/",

}

Rai, TS, Cole, JC, Nelson, DM, Dikovskaya, D, McBryan, T, Faller, W, v. Tuyn, J, Morrice, N, Hewitt, RN, Brock, C, Ivanov, A, Drotar, ME, Nixon, C, Clark, W, Sansom, OJ, King, A, Blyth, K & Adams, PD 2014, 'HIRA orchestrates a non-canonical dynamic chromatin landscape in senescence and is required for suppression of neoplasia', Epigenetics & Chromatin CSHL 2014, Cold Spring Harbor, United States, 9/09/14 - 13/09/14.

TY - CONF

T1 - HIRA orchestrates a non-canonical dynamic chromatin landscape in senescence and is required for suppression of neoplasia

AU - Rai, Taranjit Singh

AU - Cole, John C.

AU - Nelson, David M.

AU - Dikovskaya, Dina

AU - McBryan, Tony

AU - Faller, William

AU - v. Tuyn, John

AU - Morrice, Nicholas

AU - Hewitt, Rachael N.

AU - Brock, Claire

AU - Ivanov, Andrejs

AU - Drotar, Mark E.

AU - Nixon, Colin

AU - Clark, William

AU - Sansom, Owen J.

AU - King, Ayala

AU - Blyth, Karen

AU - Adams, Peter D.

PY - 2014/9/9

Y1 - 2014/9/9

N2 - Cellular senescence is a stable proliferation arrest that suppresses tumorigenesis. Cell senescence and associated tumor suppression depend on control of chromatin. Chromatin is dynamically controlled, and its imbalance can promote cancer, as evidenced by recurrent mutations and dysregulation in cancer of H3.3, a histone variant enriched at dynamic chromatin regulatory sites. Hence, it is important to understand the impact of dynamic chromatin control on tumor suppression. We show that non-proliferating tumor suppressive senescent cells express and incorporate histone H3.3 and normally "replication-dependent" histones into a non-canonical, H4K16ac-decorated, dynamic chromatin landscape. A key regulator of this landscape, histone chaperone HIRA, is required for suppression of oncogene-induced neoplasia in vivo. These results indicate a role for a non-canonical, dynamic chromatin landscape in tumor suppression.

AB - Cellular senescence is a stable proliferation arrest that suppresses tumorigenesis. Cell senescence and associated tumor suppression depend on control of chromatin. Chromatin is dynamically controlled, and its imbalance can promote cancer, as evidenced by recurrent mutations and dysregulation in cancer of H3.3, a histone variant enriched at dynamic chromatin regulatory sites. Hence, it is important to understand the impact of dynamic chromatin control on tumor suppression. We show that non-proliferating tumor suppressive senescent cells express and incorporate histone H3.3 and normally "replication-dependent" histones into a non-canonical, H4K16ac-decorated, dynamic chromatin landscape. A key regulator of this landscape, histone chaperone HIRA, is required for suppression of oncogene-induced neoplasia in vivo. These results indicate a role for a non-canonical, dynamic chromatin landscape in tumor suppression.

M3 - Poster

T2 - Epigenetics & Chromatin CSHL 2014

Y2 - 9 September 2014 through 13 September 2014

ER -

HIRA orchestrates a non-canonical dynamic chromatin landscape in senescence and is required for suppression of neoplasia

Abstract

Conference

UN SDGs

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