Effect of chloramphenicol, antimycin A and hydroxamate on the morphogenetic development of the dimorphic ascomycete Endomycopsis capsularis.
Mitochondrial protein synthesis, primary (antimycin-sensitive) respiration and secondary (antimycin-insensitive, salicyl-hydroxamate-sensitive) respiration, have been characterized in the dimorphic yeast Endomycopsis capsularis. The inhibition by chloramphenicol (CAP) of the morphogenetic development from the yeast-like form to the mycelial structure in this yeast could represent the intervention in the morphogenetic process of mitochondrial protein synthesis, since chloramphenicol blocks in vivo and in vitro mitochondrial protein synthesis. In fact, other functions such as primary and secondary respiration, do not seem to play a role in the morphogenetic development since their inhibition by antimycin A (AA) or by salicyl-hydroxamic acid (SHAM) does not affect the process. In addition, mitochondrial protein synthesis has been shown to be uninhibited by the two respiratory inhibitors.
D000968:Antimycin A / Q000494:pharmacology*; D001203:Ascomycota / Q000187:drug effects*; D002701:Chloramphenicol / Q000494:pharmacology*; D003470:Culture Media; D005656:Fungal Proteins / Q000096:biosynthesis; D006877:Hydroxamic Acids / Q000494:pharmacology*; D008928:Mitochondria / Q000187:drug effects; D009024:Morphogenesis / Q000187:drug effects; D010101:Oxygen Consumption / Q000187:drug effects; D004718:Saccharomycetales / Q000187:drug effects* / Q000254:growth & development / Q000378:metabolism
D003470:Culture Media; D005656:Fungal Proteins; D006877:Hydroxamic Acids; D000968:Antimycin A; D002701:Chloramphenicol