Abstract
Lamins form stable filaments at the nuclear periphery in metazoans. Unlike B-type lamins, lamins A and C localize also in the nuclear interior, where they interact with lamin-associated polypeptide 2 alpha (LAP2a). Using antibody labeling, we previously observed a depletion of nucleoplasmic A-type lamins in mouse cells lacking LAP2a. Here we show that loss of LAP2a actually causes formation of larger, biochemically stable lamin A/C structures in the nuclear interior that are inaccessible to lamin A/C antibodies. While nucleoplasmic lamin A forms from newly expressed pre-lamin A during processing and from soluble mitotic lamins in a LAP2a-independent manner, binding of LAP2a to lamins A/C during interphase inhibits formation of higher order structures, keeping nucleoplasmic lamin A/C in a mobile state independent of lamin A/C S22 phosphorylation. We propose that LAP2a is essential to maintain a mobile lamin A/C pool in the nuclear interior, which is required for proper nuclear functions.
Article and author information
Author details
Funding
Austrian Science Fund (P26492-B20,P29713-B28,P32512-B)
- Roland Foisner
Austrian Academy of Sciences (APART 11657)
- Nana Naetar
Israel Science Foundation (ISF grant 1219/17)
- Irena Bronshtein
- Yuval Garini
European Cooperation in Science and Technology (COST-STSM-BM1002-8698,COST-STSM-BM1002-11436)
- Thomas Dechat
European Molecular Biology Organization (ASTF 316-2011)
- Thomas Dechat
S Grosskopf Grant
- Irena Bronshtein
- Yuval Garini
Austrian Academy of Sciences (ÖAW DOC 25725)
- Konstantina Georgiou
The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.
Reviewing Editor
- Megan C King, Yale School of Medicine, United States
Publication history
- Received: September 28, 2020
- Accepted: February 18, 2021
- Accepted Manuscript published: February 19, 2021 (version 1)
Copyright
© 2021, Naetar et al.
This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.
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