Had1 Is Required for Cell Wall Integrity and Fungal Virulence in .

G3 (Bethesda)

School of Food Science and Biotechnology, Institute of Agricultural Science and Technology, Kyungpook National University, Daegu 41566, Republic of Korea

Published: February 2018

AI Article Synopsis

  • Research highlights the role of Had1, a calcineurin substrate, in regulating stress survival and virulence in a human fungal pathogen.
  • The Had1-deficient mutant shows growth issues at higher temperatures and increased sensitivity to cell wall stress.
  • The study finds that Had1 and the transcription factor Crz1 operate in parallel pathways affecting the pathogen's ability to survive stress and cause disease.

Article Abstract

Calcineurin modulates environmental stress survival and virulence of the human fungal pathogen Previously, we identified 44 putative calcineurin substrates, and proposed that the calcineurin pathway is branched to regulate targets including Crz1, Pbp1, and Puf4 in In this study, we characterized Had1, which is one of the putative calcineurin substrates belonging to the ubiquitously conserved haloacid dehalogenase β-phosphoglucomutase protein superfamily. Growth of the ∆ mutant was found to be compromised at 38° or higher. In addition, the ∆ mutant exhibited increased sensitivity to cell wall perturbing agents, including Congo Red and Calcofluor White, and to an endoplasmic reticulum stress inducer dithiothreitol. Virulence studies revealed that the mutation results in attenuated virulence compared to the wild-type strain in a murine inhalation infection model. Genetic epistasis analysis revealed that Had1 and the zinc finger transcription factor Crz1 play roles in parallel pathways that orchestrate stress survival and fungal virulence. Overall, our results demonstrate that Had1 is a key regulator of thermotolerance, cell wall integrity, and virulence of .

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5919746PMC
http://dx.doi.org/10.1534/g3.117.300444DOI Listing

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