Hog1 Controls Lipids Homeostasis Upon Osmotic Stress in .

J Fungi (Basel)

Departamento de Microbiología y Parasitología-IRYCIS, Facultad de Farmacia, Universidad Complutense de Madrid, Plaza de Ramón y Cajal s/n, 28040 Madrid, Spain.

Published: December 2020

AI Article Synopsis

  • The Hog1 MAPK is crucial for answering osmotic stress and also helps the pathogen deal with various other stresses, influencing its survival and ability to flourish in different environments.
  • The study reveals that Hog1 is vital for maintaining lipid balance, as mutants lacking Hog1 accumulate lipid droplets under osmotic stress, leading to cell permeability issues.
  • Cek1, another MAPK related to osmotic stress response, does not affect lipid homeostasis, suggesting that Hog1 is the primary MAP kinase managing these processes and that lipid metabolism changes make mutants more susceptible to osmotic stress.

Article Abstract

As opportunistic pathogen, adapts to different environmental conditions and its corresponding stress. The Hog1 MAPK (Mitogen Activated Protein Kinase) was identified as the main MAPK involved in the response to osmotic stress. It was later shown that this MAPK is also involved in the response to a variety of stresses and therefore, its role in virulence, survival to phagocytes and establishment as commensal in the mouse gastrointestinal tract was reported. In this work, the role of Hog1 in osmotic stress is further analyzed, showing that this MAPK is involved in lipid homeostasis. The mutant accumulates lipid droplets when exposed to osmotic stress, leading to an increase in cell permeability and delaying the endocytic trafficking routes. Cek1, a MAPK also implicated in the response to osmotic challenge, did not play a role in lipid homeostasis indicating that Hog1 is the main MAP kinase in this response. The alteration on lipid metabolism observed in mutants is proposed to contribute to the sensitivity to osmotic stress.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7770603PMC
http://dx.doi.org/10.3390/jof6040355DOI Listing

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