Open AccessCryptococcus neoformans Ca 2+ homeostasis requires a chloride channel/antiporter C lc1 in JEC 21, but not in H 99
Author(s) -
Li Dong,
Zhang Xiaojiao,
Li Zhongming,
Yang Jiao,
Pan Jiao,
Zhu Xudong
Publication year - 2012
Publication title -
fems yeast research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.991
H-Index - 92
eISSN - 1567-1364
pISSN - 1567-1356
DOI - 10.1111/j.1567-1364.2011.00763.x
Subject(s) - cryptococcus neoformans , biology , antiporter , homeostasis , chloride channel , microbiology and biotechnology , biochemistry , membrane
CLC ‐type chloride/proton antiporters are required for copper/iron homeostasis in fungi. A relationship between CLC s and Ca 2+ homeostasis has not been found before. Here we demonstrate the requirement of the antiporter CLC 1 for Ca 2+ homeostasis/signaling in C ryptococcus neoformans . The deletion of CLC1 in JEC 21 resulted in a mutant hypersensitive to cyclosporine A , an inhibitor of calcineurin. Intracellular Ca 2+ deficiency in the mutant T x1 was confirmed with F luo‐3 staining epi‐fluorescence microscopy. T x1 failed to grow at elevated temperature and in SDS and displayed defects in cell wall integrity and cell separation. This defective phenotype is because of Ca 2+ deficiency that was restorable by exogenous Ca 2+ . In contrast, H 99 CLC1 was dispensable for Ca 2+ homeostasis and had no comparable defective consequences if deleted, suggesting divergent roles of CLC s in Ca 2+ homeostasis. Distinct Ca 2+ homeostasis mechanisms may contribute the virulence difference between the two strains. This work reveals a novel action of CLC antiporters in fungi and may provide information as to the evolution of pathogenicity among cryptococcal strains.