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Stress tolerances of nullmutants of function‐unknown genes encoding menadione stress‐responsive proteins in Aspergillus nidulans
Author(s) -
Leiter Éva,
Bálint Mihály,
Miskei Márton,
Orosz Erzsébet,
Szabó Zsuzsa,
Pócsi István
Publication year - 2016
Publication title -
journal of basic microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.58
H-Index - 54
eISSN - 1521-4028
pISSN - 0233-111X
DOI - 10.1002/jobm.201500500
Subject(s) - menadione , mutant , gene , aspergillus nidulans , phenotype , biology , genetics , locus (genetics) , microbiology and biotechnology , biochemistry , oxidative stress
A group of menadione stress‐responsive function‐unkown genes of Aspergillus nidulans (Locus IDs ANID_03987.1, ANID_06058.1, ANID_10219.1, and ANID_10260.1) was deleted and phenotypically characterized. Importantly, comparative and phylogenetic analyses of the tested A. nidulans genes and their orthologs shed light only on the presence of a TANGO2 domain with NRDE protein motif in the translated ANID_06058.1 gene but did not reveal any recognizable protein‐encoding domains in other protein sequences. The gene deletion strains were subjected to oxidative, osmotic, and metal ion stress and, surprisingly, only the ΔANID_10219.1 mutant showed an increased sensitivity to 0.12 mmol l −1 menadione sodium bisulfite. The gene deletions affected the stress sensitivities (tolerances) irregularly, for example, some strains grew more slowly when exposed to various oxidants and/or osmotic stress generating agents, meanwhile the ΔANID_10260.1 mutant possessed a wild‐type tolerance to all stressors tested. Our results are in line with earlier studies demonstrating that the deletions of stress‐responsive genes do not confer necessarily any stress‐sensitivity phenotypes, which can be attributed to compensatory mechanisms based on other elements of the stress response system with overlapping functions.