Format

Send to

Choose Destination
Nat Commun. 2019 Apr 23;10(1):1871. doi: 10.1038/s41467-019-09623-x.

Nuclear membrane protein Lem2 regulates nuclear size through membrane flow.

Author information

1
Hiroshima Research Center for Healthy Aging, Department of Molecular Biotechnology, Graduate School of Advanced Sciences of Matter, Hiroshima University, Higashi-Hiroshima, 739-8530, Japan. kume513@hiroshima-u.ac.jp.
2
Cell Cycle Laboratory, The Francis Crick Institute, London, NW1 1AT, UK. kume513@hiroshima-u.ac.jp.
3
Cell Cycle Laboratory, The Francis Crick Institute, London, NW1 1AT, UK.
4
Electron Microscopy Science Technology Platform, The Francis Crick Institute, London, NW1 1AT, UK.
5
Laboratory of Yeast Genetics and Cell Biology, Rockefeller University, New York, NY, 10065, USA.

Abstract

The size of the membrane-bound nucleus scales with cell size in a wide range of cell types but the mechanisms determining overall nuclear size remain largely unknown. Here we investigate the role of fission yeast inner nuclear membrane proteins in determining nuclear size, and propose that the Lap2-Emerin-Man1 domain protein Lem2 acts as a barrier to membrane flow between the nucleus and other parts of the cellular membrane system. Lem2 deletion increases membrane flow into and out of the nuclear envelope in response to changes in membrane synthesis and nucleocytoplasmic transport, altering nuclear size. The endoplasmic reticulum protein Lnp1 acts as a secondary barrier to membrane flow, functionally compensating for lack of Lem2. We propose that this is part of the mechanism that maintains nuclear size proportional to cellular membrane content and thus to cell size. Similar regulatory principles may apply to other organelles in the eukaryotic subcellular membrane network.

PMID:
31015410
PMCID:
PMC6478680
DOI:
10.1038/s41467-019-09623-x
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Nature Publishing Group Icon for PubMed Central
Loading ...
Support Center