Histone deacetylase 8 is required for centrosome cohesion and influenza A virus entry.

Influenza A virus (IAV) enters host cells by endocytosis followed by acid-activated penetration from late endosomes (LEs). Using siRNA silencing, we found that histone deacetylase 8 (HDAC8), a cytoplasmic enzyme, efficiently promoted productive entry of IAV into tissue culture cells, whereas HDAC1 s...

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Autores principales:	Yohei Yamauchi, Heithem Boukari, Indranil Banerjee, Ivo F Sbalzarini, Peter Horvath, Ari Helenius
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2011
Materias:	Immunologic diseases. Allergy RC581-607 Biology (General) QH301-705.5
Acceso en línea:	https://doaj.org/article/80a38b8b1c574a3699c6581885e7aa07
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spelling	oai:doaj.org-article:80a38b8b1c574a3699c6581885e7aa072021-11-18T06:05:12ZHistone deacetylase 8 is required for centrosome cohesion and influenza A virus entry.1553-73661553-737410.1371/journal.ppat.1002316https://doaj.org/article/80a38b8b1c574a3699c6581885e7aa072011-10-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/22046129/pdf/?tool=EBIhttps://doaj.org/toc/1553-7366https://doaj.org/toc/1553-7374Influenza A virus (IAV) enters host cells by endocytosis followed by acid-activated penetration from late endosomes (LEs). Using siRNA silencing, we found that histone deacetylase 8 (HDAC8), a cytoplasmic enzyme, efficiently promoted productive entry of IAV into tissue culture cells, whereas HDAC1 suppressed it. HDAC8 enhanced endocytosis, acidification, and penetration of the incoming virus. In contrast, HDAC1 inhibited acidification and penetration. The effects were connected with dramatic alterations in the organization of the microtubule system, and, as a consequence, a change in the behavior of LEs and lysosomes (LYs). Depletion of HDAC8 caused loss of centrosome-associated microtubules and loss of directed centripetal movement of LEs, dispersing LE/LYs to the cell periphery. For HDAC1, the picture was the opposite. To explain these changes, centrosome cohesion emerged as the critical factor. Depletion of HDAC8 caused centrosome splitting, which could also be induced by depleting a centriole-linker protein, rootletin. In both cases, IAV infection was inhibited. HDAC1 depletion reduced the splitting of centrosomes, and enhanced infection. The longer the distance between centrosomes, the lower the level of infection. HDAC8 depletion was also found to inhibit infection of Uukuniemi virus (a bunyavirus) suggesting common requirements among late penetrating enveloped viruses. The results established class I HDACs as powerful regulators of microtubule organization, centrosome function, endosome maturation, and infection by IAV and other late penetrating viruses.Yohei YamauchiHeithem BoukariIndranil BanerjeeIvo F SbalzariniPeter HorvathAri HeleniusPublic Library of Science (PLoS)articleImmunologic diseases. AllergyRC581-607Biology (General)QH301-705.5ENPLoS Pathogens, Vol 7, Iss 10, p e1002316 (2011)
institution	DOAJ
collection	DOAJ
language	EN
topic	Immunologic diseases. Allergy RC581-607 Biology (General) QH301-705.5
spellingShingle	Immunologic diseases. Allergy RC581-607 Biology (General) QH301-705.5 Yohei Yamauchi Heithem Boukari Indranil Banerjee Ivo F Sbalzarini Peter Horvath Ari Helenius Histone deacetylase 8 is required for centrosome cohesion and influenza A virus entry.
description	Influenza A virus (IAV) enters host cells by endocytosis followed by acid-activated penetration from late endosomes (LEs). Using siRNA silencing, we found that histone deacetylase 8 (HDAC8), a cytoplasmic enzyme, efficiently promoted productive entry of IAV into tissue culture cells, whereas HDAC1 suppressed it. HDAC8 enhanced endocytosis, acidification, and penetration of the incoming virus. In contrast, HDAC1 inhibited acidification and penetration. The effects were connected with dramatic alterations in the organization of the microtubule system, and, as a consequence, a change in the behavior of LEs and lysosomes (LYs). Depletion of HDAC8 caused loss of centrosome-associated microtubules and loss of directed centripetal movement of LEs, dispersing LE/LYs to the cell periphery. For HDAC1, the picture was the opposite. To explain these changes, centrosome cohesion emerged as the critical factor. Depletion of HDAC8 caused centrosome splitting, which could also be induced by depleting a centriole-linker protein, rootletin. In both cases, IAV infection was inhibited. HDAC1 depletion reduced the splitting of centrosomes, and enhanced infection. The longer the distance between centrosomes, the lower the level of infection. HDAC8 depletion was also found to inhibit infection of Uukuniemi virus (a bunyavirus) suggesting common requirements among late penetrating enveloped viruses. The results established class I HDACs as powerful regulators of microtubule organization, centrosome function, endosome maturation, and infection by IAV and other late penetrating viruses.
format	article
author	Yohei Yamauchi Heithem Boukari Indranil Banerjee Ivo F Sbalzarini Peter Horvath Ari Helenius
author_facet	Yohei Yamauchi Heithem Boukari Indranil Banerjee Ivo F Sbalzarini Peter Horvath Ari Helenius
author_sort	Yohei Yamauchi
title	Histone deacetylase 8 is required for centrosome cohesion and influenza A virus entry.
title_short	Histone deacetylase 8 is required for centrosome cohesion and influenza A virus entry.
title_full	Histone deacetylase 8 is required for centrosome cohesion and influenza A virus entry.
title_fullStr	Histone deacetylase 8 is required for centrosome cohesion and influenza A virus entry.
title_full_unstemmed	Histone deacetylase 8 is required for centrosome cohesion and influenza A virus entry.
title_sort	histone deacetylase 8 is required for centrosome cohesion and influenza a virus entry.
publisher	Public Library of Science (PLoS)
publishDate	2011
url	https://doaj.org/article/80a38b8b1c574a3699c6581885e7aa07
work_keys_str_mv	AT yoheiyamauchi histonedeacetylase8isrequiredforcentrosomecohesionandinfluenzaavirusentry AT heithemboukari histonedeacetylase8isrequiredforcentrosomecohesionandinfluenzaavirusentry AT indranilbanerjee histonedeacetylase8isrequiredforcentrosomecohesionandinfluenzaavirusentry AT ivofsbalzarini histonedeacetylase8isrequiredforcentrosomecohesionandinfluenzaavirusentry AT peterhorvath histonedeacetylase8isrequiredforcentrosomecohesionandinfluenzaavirusentry AT arihelenius histonedeacetylase8isrequiredforcentrosomecohesionandinfluenzaavirusentry
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Histone deacetylase 8 is required for centrosome cohesion and influenza A virus entry.

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