Su(Hw) primes 66D and 7F Drosophila chorion genes loci for amplification through chromatin decondensation

Abstract Suppressor of Hairy wing [Su(Hw)] is an insulator protein that participates in regulating chromatin architecture and gene repression in Drosophila. In previous studies we have shown that Su(Hw) is also required for pre-replication complex (pre-RC) recruitment on Su(Hw)-bound sites (SBSs) in...

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Autores principales:	Nadezhda E. Vorobyeva, Maksim Erokhin, Darya Chetverina, Alexey N. Krasnov, Marina Yu. Mazina
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2021
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/9eabbf3b9f914508af1c9728605193e9
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spelling	oai:doaj.org-article:9eabbf3b9f914508af1c9728605193e92021-12-02T16:45:54ZSu(Hw) primes 66D and 7F Drosophila chorion genes loci for amplification through chromatin decondensation10.1038/s41598-021-96488-02045-2322https://doaj.org/article/9eabbf3b9f914508af1c9728605193e92021-08-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-96488-0https://doaj.org/toc/2045-2322Abstract Suppressor of Hairy wing [Su(Hw)] is an insulator protein that participates in regulating chromatin architecture and gene repression in Drosophila. In previous studies we have shown that Su(Hw) is also required for pre-replication complex (pre-RC) recruitment on Su(Hw)-bound sites (SBSs) in Drosophila S2 cells and pupa. Here, we describe the effect of Su(Hw) on developmentally regulated amplification of 66D and 7F Drosophila amplicons in follicle cells (DAFCs), widely used as models in replication studies. We show Su(Hw) binding co-localizes with all known DAFCs in Drosophila ovaries, whereas disruption of Su(Hw) binding to 66D and 7F DAFCs causes a two-fold decrease in the amplification of these loci. The complete loss of Su(Hw) binding to chromatin impairs pre-RC recruitment to all amplification regulatory regions of 66D and 7F loci at early oogenesis (prior to DAFCs amplification). These changes coincide with a considerable Su(Hw)-dependent condensation of chromatin at 66D and 7F loci. Although we observed the Brm, ISWI, Mi-2, and CHD1 chromatin remodelers at SBSs genome wide, their remodeler activity does not appear to be responsible for chromatin decondensation at the 66D and 7F amplification regulatory regions. We have discovered that, in addition to the CBP/Nejire and Chameau histone acetyltransferases, the Gcn5 acetyltransferase binds to 66D and 7F DAFCs at SBSs and this binding is dependent on Su(Hw). We propose that the main function of Su(Hw) in developmental amplification of 66D and 7F DAFCs is to establish a chromatin structure that is permissive to pre-RC recruitment.Nadezhda E. VorobyevaMaksim ErokhinDarya ChetverinaAlexey N. KrasnovMarina Yu. MazinaNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-14 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Nadezhda E. Vorobyeva Maksim Erokhin Darya Chetverina Alexey N. Krasnov Marina Yu. Mazina Su(Hw) primes 66D and 7F Drosophila chorion genes loci for amplification through chromatin decondensation
description	Abstract Suppressor of Hairy wing [Su(Hw)] is an insulator protein that participates in regulating chromatin architecture and gene repression in Drosophila. In previous studies we have shown that Su(Hw) is also required for pre-replication complex (pre-RC) recruitment on Su(Hw)-bound sites (SBSs) in Drosophila S2 cells and pupa. Here, we describe the effect of Su(Hw) on developmentally regulated amplification of 66D and 7F Drosophila amplicons in follicle cells (DAFCs), widely used as models in replication studies. We show Su(Hw) binding co-localizes with all known DAFCs in Drosophila ovaries, whereas disruption of Su(Hw) binding to 66D and 7F DAFCs causes a two-fold decrease in the amplification of these loci. The complete loss of Su(Hw) binding to chromatin impairs pre-RC recruitment to all amplification regulatory regions of 66D and 7F loci at early oogenesis (prior to DAFCs amplification). These changes coincide with a considerable Su(Hw)-dependent condensation of chromatin at 66D and 7F loci. Although we observed the Brm, ISWI, Mi-2, and CHD1 chromatin remodelers at SBSs genome wide, their remodeler activity does not appear to be responsible for chromatin decondensation at the 66D and 7F amplification regulatory regions. We have discovered that, in addition to the CBP/Nejire and Chameau histone acetyltransferases, the Gcn5 acetyltransferase binds to 66D and 7F DAFCs at SBSs and this binding is dependent on Su(Hw). We propose that the main function of Su(Hw) in developmental amplification of 66D and 7F DAFCs is to establish a chromatin structure that is permissive to pre-RC recruitment.
format	article
author	Nadezhda E. Vorobyeva Maksim Erokhin Darya Chetverina Alexey N. Krasnov Marina Yu. Mazina
author_facet	Nadezhda E. Vorobyeva Maksim Erokhin Darya Chetverina Alexey N. Krasnov Marina Yu. Mazina
author_sort	Nadezhda E. Vorobyeva
title	Su(Hw) primes 66D and 7F Drosophila chorion genes loci for amplification through chromatin decondensation
title_short	Su(Hw) primes 66D and 7F Drosophila chorion genes loci for amplification through chromatin decondensation
title_full	Su(Hw) primes 66D and 7F Drosophila chorion genes loci for amplification through chromatin decondensation
title_fullStr	Su(Hw) primes 66D and 7F Drosophila chorion genes loci for amplification through chromatin decondensation
title_full_unstemmed	Su(Hw) primes 66D and 7F Drosophila chorion genes loci for amplification through chromatin decondensation
title_sort	su(hw) primes 66d and 7f drosophila chorion genes loci for amplification through chromatin decondensation
publisher	Nature Portfolio
publishDate	2021
url	https://doaj.org/article/9eabbf3b9f914508af1c9728605193e9
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Su(Hw) primes 66D and 7F Drosophila chorion genes loci for amplification through chromatin decondensation

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