Gv1, a Zinc Finger Gene Controlling Endogenous MLV Expression.

Autor:	Young GR; Retrovirus-host Interactions Laboratory, The Francis Crick Institute, London, UK., Ferron AKW; Retrovirus-host Interactions Laboratory, The Francis Crick Institute, London, UK., Panova V; Retroviral Immunology, The Francis Crick Institute, London, UK., Eksmond U; Retroviral Immunology, The Francis Crick Institute, London, UK., Oliver PL; MRC Harwell Institute, Harwell Campus, Oxfordshire, UK., Kassiotis G; Retroviral Immunology, The Francis Crick Institute, London, UK.; Department of Infectious Disease, Imperial College London, London, UK., Stoye JP; Retrovirus-host Interactions Laboratory, The Francis Crick Institute, London, UK.; Department of Infectious Disease, Imperial College London, London, UK.
Jazyk:	angličtina
Zdroj:	Molecular biology and evolution [Mol Biol Evol] 2021 May 19; Vol. 38 (6), pp. 2468-2474.
DOI:	10.1093/molbev/msab039
Abstrakt:	The genomes of inbred mice harbor around 50 endogenous murine leukemia virus (MLV) loci, although the specific complement varies greatly between strains. The Gv1 locus is known to control the transcription of endogenous MLVs and to be the dominant determinant of cell-surface presentation of MLV envelope, the GIX antigen. Here, we identify a single Krüppel-associated box zinc finger protein (ZFP) gene, Zfp998, as Gv1 and show it to be necessary and sufficient to determine the GIX+ phenotype. By long-read sequencing of bacterial artificial chromosome clones from 129 mice, the prototypic GIX+ strain, we reveal the source of sufficiency and deficiency as splice-acceptor variations and highlight the varying origins of the chromosomal region encompassing Gv1. Zfp998 becomes the second identified ZFP gene responsible for epigenetic suppression of endogenous MLVs in mice and further highlights the prominent role of this gene family in control of endogenous retroviruses. (© The Author(s) 2021. Published by Oxford University Press on behalf of the Society for Molecular Biology and Evolution.)
Databáze:	MEDLINE
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