Mitochondrial activity and heat-shock response during morphogenesis in the pathogenic fungus Histoplasma capsulatum

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Abstract
Changes in temperature and a variety of other stimuli coordinately induce transcription of a specific set of heat-shock genes in all organisms. In the human fungal pathogen Histoplasma capsulatum, a temperature shift from 25 to 37 °C acts not only as a signal that causes transcription of heat-shock genes, but also triggers a morphological mycelium-to yeast-phase transition. The temperature-induced morphological transition may be viewed as a heat-shock response followed by cellular adaptation to a higher temperature. We have found that by inducing thermotolerance, i.e., an initial incubation at 34 °C, the thermosensitive attenuated Downs strain of H. capsulatum can be made to resemble those of the more temperature-tolerant G222B strain with respect to mitochondrial ATPase activity and electron transport efficiency at elevated temperatures. Furthermore, if the heat-shock response is first elicited by preincubation at milder temperatures or stress, transcription of heat-shock mRNA in mycelial cells of Downs strain that shifted to 37 °C proceeds at rates comparable to those of the virulent strains.Key words: heat shock, thermotolerance, ATPase, 70-kilodalton heat-shock protein, fungal morphogenesis.

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