Mechanosensitive channels Msy1 and Msy2 are required for maintaining organelle integrity upon hypoosmotic shock in
Yoshitaka Nakayama1, Aiko Hirata, Hidetoshi Iida
1Department of Biology, Tokyo Gakugei University, Koganei-shi, Tokyo, Japan.
Abstract:
The mechanosensitive channels, Mys1 and Msy2, in fission yeast are localized in the endoplasmic reticulum membrane and control cytoplasmic Ca(2+) levels in the hypoosmotic response. We here investigated changes in organellar structures with hypoosmotic shock using transmission electron microscopy. While msy1(-) and msy2(-) single mutant cells developed a number of swollen vacuoles following hypoosmotic shock, similar to wild-type cells, msy1(-) msy2(-) double mutant cells only had two abnormally large vacuoles and cracks between the inner and outer nuclear membranes. These results suggest that Msy1 and Msy2 may be involved in maintaining vacuole integrity and protecting the nuclear envelope upon hypoosmotic shock and also that these two channels are functionally complementary.
Insights
Mechanosensitive channels Mys1 and Msy2 in fission yeast are crucial for maintaining cell structure during hypoosmotic shock. Double mutants lacking both channels exhibit severe vacuole and nuclear envelope defects, highlighting their complementary roles.
Area of Science:
- Cell Biology
- Biophysics
- Molecular Biology
Background:
- Mechanosensitive channels regulate cellular responses to mechanical stress.
- In fission yeast, Mys1 and Msy2 are endoplasmic reticulum-localized channels involved in hypoosmotic shock response.
- Cytoplasmic calcium levels are critical during osmotic stress.
Purpose of the Study:
- To investigate the role of Mys1 and Msy2 in maintaining organellar structure under hypoosmotic conditions.
- To determine the functional relationship between Mys1 and Msy2 in response to osmotic stress.
Main Methods:
- Transmission electron microscopy was used to examine organellar structures.
- Fission yeast strains with single and double mutations in Mys1 and Msy2 were subjected to hypoosmotic shock.
Main Results:
- Single mutants (msy1(-) and msy2(-)) showed swollen vacuoles, similar to wild-type cells.
- Double mutants (msy1(-) msy2(-)) displayed abnormally large vacuoles and cracks in the nuclear envelope.
- These defects suggest a critical role for both channels in maintaining cellular integrity.
Conclusions:
- Mys1 and Msy2 are essential for maintaining vacuole integrity during hypoosmotic shock.
- These channels play a role in protecting the nuclear envelope from osmotic stress.
- Msy1 and Msy2 exhibit functional complementarity in responding to hypoosmotic stress.
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