Bridgin connects the outer kinetochore to centromeric chromatin.
Bridgin connects the outer kinetochore to centromeric chromatin.
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DOI:
10.1038/s41467-020-20161-9
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发表时间:
2021-01-08
影响因子:
16.6
通讯作者:
Sanyal K
中科院分区:
文献类型:
--
作者:
Sridhar S;Hori T;Nakagawa R;Fukagawa T;Sanyal K
The microtubule-binding outer kinetochore is coupled to centromeric chromatin through CENP-CMif2, CENP-TCnn1, and CENP-UAme1 linker pathways originating from the constitutive centromere associated network (CCAN) of the inner kinetochore. Here, we demonstrate the recurrent loss of most CCAN components, including certain kinetochore linkers during the evolution of the fungal phylum of Basidiomycota. By kinetochore interactome analyses in a model basidiomycete and human pathogen Cryptococcus neoformans, a forkhead-associated domain containing protein “bridgin” was identified as a kinetochore component along with other predicted kinetochore proteins. In vivo and in vitro functional analyses of bridgin reveal its ability to connect the outer kinetochore with centromeric chromatin to ensure accurate chromosome segregation. Unlike established CCAN-based linkers, bridgin is recruited at the outer kinetochore establishing its role as a distinct family of kinetochore proteins. Presence of bridgin homologs in non-fungal lineages suggests an ancient divergent strategy exists to bridge the outer kinetochore with centromeric chromatin. The kinetochore is a multi-complex structure that helps attach chromosomes to spindle microtubules, ensuring accurate chromosome segregation during cell division. Kinetochores are thought to be evolutionarily conserved, but which components are conserved is unclear. Here, the authors report that some members of the fungal phylum of Basidomycota lack many conventional kinetochore linker proteins. Instead, they possess a human Ki67-like protein that bridges the outer part of the kinetochore to centromere DNA, which may compensate for the loss of a conventional linker.
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影响因子:
14.9
作者:
Grigoriev IV;Nikitin R;Haridas S;Kuo A;Ohm R;Otillar R;Riley R;Salamov A;Zhao X;Korzeniewski F;Smirnova T;Nordberg H;Dubchak I;Shabalov I
通讯作者:
Shabalov I
影响因子:
7.7
作者:
Drinnenberg IA;deYoung D;Henikoff S;Malik HS
通讯作者:
Malik HS
影响因子:
64.5
作者:
Akiyoshi B;Gull K
通讯作者:
Gull K
DOI:
10.1016/bs.enz.2016.03.003
发表时间:
2016
期刊:
The Enzymes
影响因子:
--
作者:
Boehm EM;Gildenberg MS;Washington MT
通讯作者:
Washington MT
影响因子:
14.9
作者:
Dubin, Manu;Fuchs, Joerg;Nellen, Wolfgang
通讯作者:
Nellen, Wolfgang