60
Views
1
CrossRef citations to date
0
Altmetric
Articles

Critical events leading to cellular mortality of yeast cells following hydrostatic pressure treatment

, , & ORCID Icon
Pages 267-272 | Received 26 Oct 2018, Accepted 28 Nov 2018, Published online: 09 Dec 2018
 

ABSTRACT

Hydrostatic pressures of 40–150 MPa are sub-lethal conditions for yeast cells. On exposure to this pressure range, damaged yeast cells will attempt to recover, but a critical cellular event may ultimately lead to cell mortality. We employed yeast strains whose cellular organelles were labeled with green fluorescent protein to investigate this critical event. We were able to visualize the nuclear membrane, nucleus, endoplasmic reticulum, Golgi body, and plasma membranes. Of the cellular organelles tested, the nuclear membrane was the weakest, displaying damage following only 50 MPa of pressure. This nuclear membrane rupture correlated with cellular viability. Thus, we hypothesize that nuclear membrane damage is the critical event leading to cellular mortality of yeast cells following hydrostatic pressure treatment.

Acknowledgement

We would like to thank Prof. Fumiyoshi Abe for the kind gift of Plasmid pPTR2-4K>R-GFP.

Disclosure statement

No potential conflict of interest was reported by the authors.

Log in via your institution

Log in to Taylor & Francis Online

PDF download + Online access

  • 48 hours access to article PDF & online version
  • Article PDF can be downloaded
  • Article PDF can be printed
USD 61.00 Add to cart

Issue Purchase

  • 30 days online access to complete issue
  • Article PDFs can be downloaded
  • Article PDFs can be printed
USD 1,965.00 Add to cart

* Local tax will be added as applicable

Related Research

People also read lists articles that other readers of this article have read.

Recommended articles lists articles that we recommend and is powered by our AI driven recommendation engine.

Cited by lists all citing articles based on Crossref citations.
Articles with the Crossref icon will open in a new tab.