Nuclear translocation of p19INK4d in response to oxidative DNA damage promotes chromatin relaxation

DNA is continuously exposed to damaging agents that can lead to changes in the genetic information with adverse consequences. Nonetheless, eukaryotic cells have mechanisms such as the DNA damage response (DDR) to prevent genomic instability. The DNA of eukaryotic cells is packaged into nucleosomes,...

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Autores principales:	Sonzogni, S.V., Ogara, M.F., Castillo, D.S., Sirkin, P.F., Radicella, J.P., Cánepa, E.T.
Formato:	JOUR
Materias:	Chromatin relaxation DNA damage response Genome integrity p19INK4d cyclin dependent kinase inhibitor 2D nuclear protein restriction endonuclease chromatin green fluorescent protein protein binding animal cell Article cell nucleus cell survival chromatin structure controlled study DNA damage DNA repair genetic stability genomic instability human human cell intracellular transport nonhuman oxidative stress protein DNA binding protein DNA interaction protein function protein transport active transport animal cell line confocal microscopy genetics HEK293 cell line HeLa cell line metabolism Northern blotting Western blotting Eukaryota Active Transport, Cell Nucleus Animals Blotting, Northern Blotting, Western Cell Line Cell Nucleus Chromatin Cyclin-Dependent Kinase Inhibitor p19 DNA Damage DNA Repair Green Fluorescent Proteins HEK293 Cells HeLa Cells Humans Microscopy, Confocal Oxidative Stress Protein Binding
Acceso en línea:	http://hdl.handle.net/20.500.12110/paper_03008177_v398_n1-2_p63_Sonzogni
Aporte de:	Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA) de Universidad de Buenos Aires

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spelling	todo:paper_03008177_v398_n1-2_p63_Sonzogni2023-10-03T15:17:48Z Nuclear translocation of p19INK4d in response to oxidative DNA damage promotes chromatin relaxation Sonzogni, S.V. Ogara, M.F. Castillo, D.S. Sirkin, P.F. Radicella, J.P. Cánepa, E.T. Chromatin relaxation DNA damage response Genome integrity p19INK4d cyclin dependent kinase inhibitor 2D nuclear protein restriction endonuclease chromatin cyclin dependent kinase inhibitor 2D green fluorescent protein protein binding animal cell Article cell nucleus cell survival chromatin structure controlled study DNA damage DNA damage response DNA repair genetic stability genomic instability human human cell intracellular transport nonhuman oxidative stress protein DNA binding protein DNA interaction protein function protein transport active transport animal cell line cell nucleus chromatin confocal microscopy genetics HEK293 cell line HeLa cell line metabolism Northern blotting oxidative stress Western blotting Eukaryota Active Transport, Cell Nucleus Animals Blotting, Northern Blotting, Western Cell Line Cell Nucleus Chromatin Cyclin-Dependent Kinase Inhibitor p19 DNA Damage DNA Repair Green Fluorescent Proteins HEK293 Cells HeLa Cells Humans Microscopy, Confocal Oxidative Stress Protein Binding DNA is continuously exposed to damaging agents that can lead to changes in the genetic information with adverse consequences. Nonetheless, eukaryotic cells have mechanisms such as the DNA damage response (DDR) to prevent genomic instability. The DNA of eukaryotic cells is packaged into nucleosomes, which fold the genome into highly condensed chromatin, but relatively little is known about the role of chromatin accessibility in DNA repair. p19INK4d, a cyclin-dependent kinase inhibitor, plays an important role in cell cycle regulation and cellular DDR. Extensive data indicate that p19INK4d is a critical factor in the maintenance of genomic integrity and cell survival. p19INK4d is upregulated by various genotoxics, improving the repair efficiency for a variety of DNA lesions. The evidence of p19INK4d translocation into the nucleus and its low sequence specificity in its interaction with DNA prompted us to hypothesize that p19INK4d plays a role at an early stage of cellular DDR. In the present study, we demonstrate that upon oxidative DNA damage, p19INK4d strongly binds to and relaxes chromatin. Furthermore, in vitro accessibility assays show that DNA is more accessible to a restriction enzyme when a chromatinized plasmid is incubated in the presence of a protein extract with high levels of p19INK4d. Nuclear protein extracts from cells overexpressing p19INK4d are better able to repair a chromatinized and damaged plasmid. These observations support the notion that p19INK4d would act as a chromatin accessibility factor that allows the access of the repair machinery to the DNA damage site. © 2014, Springer Science+Business Media New York. JOUR info:eu-repo/semantics/openAccess http://creativecommons.org/licenses/by/2.5/ar http://hdl.handle.net/20.500.12110/paper_03008177_v398_n1-2_p63_Sonzogni
institution	Universidad de Buenos Aires
institution_str	I-28
repository_str	R-134
collection	Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA)
topic	Chromatin relaxation DNA damage response Genome integrity p19INK4d cyclin dependent kinase inhibitor 2D nuclear protein restriction endonuclease chromatin cyclin dependent kinase inhibitor 2D green fluorescent protein protein binding animal cell Article cell nucleus cell survival chromatin structure controlled study DNA damage DNA damage response DNA repair genetic stability genomic instability human human cell intracellular transport nonhuman oxidative stress protein DNA binding protein DNA interaction protein function protein transport active transport animal cell line cell nucleus chromatin confocal microscopy genetics HEK293 cell line HeLa cell line metabolism Northern blotting oxidative stress Western blotting Eukaryota Active Transport, Cell Nucleus Animals Blotting, Northern Blotting, Western Cell Line Cell Nucleus Chromatin Cyclin-Dependent Kinase Inhibitor p19 DNA Damage DNA Repair Green Fluorescent Proteins HEK293 Cells HeLa Cells Humans Microscopy, Confocal Oxidative Stress Protein Binding
spellingShingle	Chromatin relaxation DNA damage response Genome integrity p19INK4d cyclin dependent kinase inhibitor 2D nuclear protein restriction endonuclease chromatin cyclin dependent kinase inhibitor 2D green fluorescent protein protein binding animal cell Article cell nucleus cell survival chromatin structure controlled study DNA damage DNA damage response DNA repair genetic stability genomic instability human human cell intracellular transport nonhuman oxidative stress protein DNA binding protein DNA interaction protein function protein transport active transport animal cell line cell nucleus chromatin confocal microscopy genetics HEK293 cell line HeLa cell line metabolism Northern blotting oxidative stress Western blotting Eukaryota Active Transport, Cell Nucleus Animals Blotting, Northern Blotting, Western Cell Line Cell Nucleus Chromatin Cyclin-Dependent Kinase Inhibitor p19 DNA Damage DNA Repair Green Fluorescent Proteins HEK293 Cells HeLa Cells Humans Microscopy, Confocal Oxidative Stress Protein Binding Sonzogni, S.V. Ogara, M.F. Castillo, D.S. Sirkin, P.F. Radicella, J.P. Cánepa, E.T. Nuclear translocation of p19INK4d in response to oxidative DNA damage promotes chromatin relaxation
topic_facet	Chromatin relaxation DNA damage response Genome integrity p19INK4d cyclin dependent kinase inhibitor 2D nuclear protein restriction endonuclease chromatin cyclin dependent kinase inhibitor 2D green fluorescent protein protein binding animal cell Article cell nucleus cell survival chromatin structure controlled study DNA damage DNA damage response DNA repair genetic stability genomic instability human human cell intracellular transport nonhuman oxidative stress protein DNA binding protein DNA interaction protein function protein transport active transport animal cell line cell nucleus chromatin confocal microscopy genetics HEK293 cell line HeLa cell line metabolism Northern blotting oxidative stress Western blotting Eukaryota Active Transport, Cell Nucleus Animals Blotting, Northern Blotting, Western Cell Line Cell Nucleus Chromatin Cyclin-Dependent Kinase Inhibitor p19 DNA Damage DNA Repair Green Fluorescent Proteins HEK293 Cells HeLa Cells Humans Microscopy, Confocal Oxidative Stress Protein Binding
description	DNA is continuously exposed to damaging agents that can lead to changes in the genetic information with adverse consequences. Nonetheless, eukaryotic cells have mechanisms such as the DNA damage response (DDR) to prevent genomic instability. The DNA of eukaryotic cells is packaged into nucleosomes, which fold the genome into highly condensed chromatin, but relatively little is known about the role of chromatin accessibility in DNA repair. p19INK4d, a cyclin-dependent kinase inhibitor, plays an important role in cell cycle regulation and cellular DDR. Extensive data indicate that p19INK4d is a critical factor in the maintenance of genomic integrity and cell survival. p19INK4d is upregulated by various genotoxics, improving the repair efficiency for a variety of DNA lesions. The evidence of p19INK4d translocation into the nucleus and its low sequence specificity in its interaction with DNA prompted us to hypothesize that p19INK4d plays a role at an early stage of cellular DDR. In the present study, we demonstrate that upon oxidative DNA damage, p19INK4d strongly binds to and relaxes chromatin. Furthermore, in vitro accessibility assays show that DNA is more accessible to a restriction enzyme when a chromatinized plasmid is incubated in the presence of a protein extract with high levels of p19INK4d. Nuclear protein extracts from cells overexpressing p19INK4d are better able to repair a chromatinized and damaged plasmid. These observations support the notion that p19INK4d would act as a chromatin accessibility factor that allows the access of the repair machinery to the DNA damage site. © 2014, Springer Science+Business Media New York.
format	JOUR
author	Sonzogni, S.V. Ogara, M.F. Castillo, D.S. Sirkin, P.F. Radicella, J.P. Cánepa, E.T.
author_facet	Sonzogni, S.V. Ogara, M.F. Castillo, D.S. Sirkin, P.F. Radicella, J.P. Cánepa, E.T.
author_sort	Sonzogni, S.V.
title	Nuclear translocation of p19INK4d in response to oxidative DNA damage promotes chromatin relaxation
title_short	Nuclear translocation of p19INK4d in response to oxidative DNA damage promotes chromatin relaxation
title_full	Nuclear translocation of p19INK4d in response to oxidative DNA damage promotes chromatin relaxation
title_fullStr	Nuclear translocation of p19INK4d in response to oxidative DNA damage promotes chromatin relaxation
title_full_unstemmed	Nuclear translocation of p19INK4d in response to oxidative DNA damage promotes chromatin relaxation
title_sort	nuclear translocation of p19ink4d in response to oxidative dna damage promotes chromatin relaxation
url	http://hdl.handle.net/20.500.12110/paper_03008177_v398_n1-2_p63_Sonzogni
work_keys_str_mv	AT sonzognisv nucleartranslocationofp19ink4dinresponsetooxidativednadamagepromoteschromatinrelaxation AT ogaramf nucleartranslocationofp19ink4dinresponsetooxidativednadamagepromoteschromatinrelaxation AT castillods nucleartranslocationofp19ink4dinresponsetooxidativednadamagepromoteschromatinrelaxation AT sirkinpf nucleartranslocationofp19ink4dinresponsetooxidativednadamagepromoteschromatinrelaxation AT radicellajp nucleartranslocationofp19ink4dinresponsetooxidativednadamagepromoteschromatinrelaxation AT canepaet nucleartranslocationofp19ink4dinresponsetooxidativednadamagepromoteschromatinrelaxation
_version_	1782030567753121792

Nuclear translocation of p19INK4d in response to oxidative DNA damage promotes chromatin relaxation

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