Selenocystine-resistant mutants of Histoplasma capsulatum.
Cysteine metabolism has been thought to be important to the phenomenon of dimorphism in Histoplasma capsulatum. We sought mutants with genetic blocks in the metabolism of cysteine by selection of colonies resistant to the toxic analogue, selenocystine. The 22 resistant strains thus obtained were all deficient in uptake of cystine from the surrounding medium but were normally able to convert from mycelium to yeast and back again. Furthermore, they had normal quantities of NADH-dependent cystine reductase when this enzyme was measured. We conclude that mutants defective in cystine uptake can be readily obtained by selection of colonies resistant to selenocystine, and that a lesion in cystine-uptake does not appear to affect the phenomenon of dimorphism in this organism.
D003553:Cystine / Q000031:analogs & derivatives* / Q000378:metabolism* / Q000494:pharmacology; D004352:Drug Resistance, Microbial; D006658:Histoplasma / Q000187:drug effects* / Q000235:genetics / Q000378:metabolism; D009154:Mutation; D009247:NADH, NADPH Oxidoreductases / Q000378:metabolism; D016566:Organoselenium Compounds; D012643:Selenium / Q000494:pharmacology*
D016566:Organoselenium Compounds; C009226:selenocystine; D003553:Cystine; D009247:NADH, NADPH Oxidoreductases; C019976:Cystine reductase; D012643:Selenium