Mad1's ability to interact with Mad2 is essential to regulate and monitor meiotic synapsis in C. elegans.

Meiotic homolog synapsis is essential to ensure accurate segregation of chromosomes during meiosis. In C. elegans, proper regulation of synapsis and a checkpoint that monitors synapsis relies on the spindle checkpoint components, Mad1 and Mad2, and Pairing Centers (PCs), cis-acting loci that interac...

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Autores principales:	Alice Devigne, Needhi Bhalla
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2021
Materias:	Genetics QH426-470
Acceso en línea:	https://doaj.org/article/8172bf6758db40e384b043d3d26addb4
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spelling	oai:doaj.org-article:8172bf6758db40e384b043d3d26addb42021-12-02T20:03:26ZMad1's ability to interact with Mad2 is essential to regulate and monitor meiotic synapsis in C. elegans.1553-73901553-740410.1371/journal.pgen.1009598https://doaj.org/article/8172bf6758db40e384b043d3d26addb42021-11-01T00:00:00Zhttps://doi.org/10.1371/journal.pgen.1009598https://doaj.org/toc/1553-7390https://doaj.org/toc/1553-7404Meiotic homolog synapsis is essential to ensure accurate segregation of chromosomes during meiosis. In C. elegans, proper regulation of synapsis and a checkpoint that monitors synapsis relies on the spindle checkpoint components, Mad1 and Mad2, and Pairing Centers (PCs), cis-acting loci that interact with the nuclear envelope to mobilize chromosomes within the nucleus. Here, we test what specific functions of Mad1 and Mad2 are required to regulate and monitor synapsis. We find that a mutation that prevents Mad1's localization to the nuclear periphery abolishes the synapsis checkpoint but has no effect on Mad2's localization to the nuclear periphery or synapsis. By contrast, a mutation that prevents Mad1's interaction with Mad2 abolishes the synapsis checkpoint, delays synapsis and fails to localize Mad2 to the nuclear periphery. These data indicate that Mad1's primary role in regulating synapsis is through control of Mad2 and that Mad2 can bind other factors at the nuclear periphery. We also tested whether Mad2's ability to adopt a specific conformation associated with its activity during spindle checkpoint function is required for its role in meiosis. A mutation that prevents Mad2 from adopting its active conformer fails to localize to the nuclear periphery, abolishes the synapsis checkpoint and exhibits substantial defects in meiotic synapsis. Thus, Mad2, and its regulation by Mad1, is an important regulator of meiotic synapsis in C. elegans.Alice DevigneNeedhi BhallaPublic Library of Science (PLoS)articleGeneticsQH426-470ENPLoS Genetics, Vol 17, Iss 11, p e1009598 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Genetics QH426-470
spellingShingle	Genetics QH426-470 Alice Devigne Needhi Bhalla Mad1's ability to interact with Mad2 is essential to regulate and monitor meiotic synapsis in C. elegans.
description	Meiotic homolog synapsis is essential to ensure accurate segregation of chromosomes during meiosis. In C. elegans, proper regulation of synapsis and a checkpoint that monitors synapsis relies on the spindle checkpoint components, Mad1 and Mad2, and Pairing Centers (PCs), cis-acting loci that interact with the nuclear envelope to mobilize chromosomes within the nucleus. Here, we test what specific functions of Mad1 and Mad2 are required to regulate and monitor synapsis. We find that a mutation that prevents Mad1's localization to the nuclear periphery abolishes the synapsis checkpoint but has no effect on Mad2's localization to the nuclear periphery or synapsis. By contrast, a mutation that prevents Mad1's interaction with Mad2 abolishes the synapsis checkpoint, delays synapsis and fails to localize Mad2 to the nuclear periphery. These data indicate that Mad1's primary role in regulating synapsis is through control of Mad2 and that Mad2 can bind other factors at the nuclear periphery. We also tested whether Mad2's ability to adopt a specific conformation associated with its activity during spindle checkpoint function is required for its role in meiosis. A mutation that prevents Mad2 from adopting its active conformer fails to localize to the nuclear periphery, abolishes the synapsis checkpoint and exhibits substantial defects in meiotic synapsis. Thus, Mad2, and its regulation by Mad1, is an important regulator of meiotic synapsis in C. elegans.
format	article
author	Alice Devigne Needhi Bhalla
author_facet	Alice Devigne Needhi Bhalla
author_sort	Alice Devigne
title	Mad1's ability to interact with Mad2 is essential to regulate and monitor meiotic synapsis in C. elegans.
title_short	Mad1's ability to interact with Mad2 is essential to regulate and monitor meiotic synapsis in C. elegans.
title_full	Mad1's ability to interact with Mad2 is essential to regulate and monitor meiotic synapsis in C. elegans.
title_fullStr	Mad1's ability to interact with Mad2 is essential to regulate and monitor meiotic synapsis in C. elegans.
title_full_unstemmed	Mad1's ability to interact with Mad2 is essential to regulate and monitor meiotic synapsis in C. elegans.
title_sort	mad1's ability to interact with mad2 is essential to regulate and monitor meiotic synapsis in c. elegans.
publisher	Public Library of Science (PLoS)
publishDate	2021
url	https://doaj.org/article/8172bf6758db40e384b043d3d26addb4
work_keys_str_mv	AT alicedevigne mad1sabilitytointeractwithmad2isessentialtoregulateandmonitormeioticsynapsisincelegans AT needhibhalla mad1sabilitytointeractwithmad2isessentialtoregulateandmonitormeioticsynapsisincelegans
_version_	1718375669863284736

Mad1's ability to interact with Mad2 is essential to regulate and monitor meiotic synapsis in C. elegans.

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