Small GTPase Rac promotes hyphal formation and microconidiogenesis in Trichophyton rubrum.

Abstract

Morphogenesis plays a pivotal role in the infection process of Trichophyton rubrum, a primary aetiological agent of dermatophytosis that inhabits superficial human tissues. T. rubrum proliferates by extending filamentous structures, or hyphae, which are composed of highly polarized cells. In response to environmental stimuli, T. rubrum also produces asexual spores called microconidia, consisting of individual cells. Although these dynamic morphological changes are critical for T. rubrum proliferation and environmental adaptation, the molecular mechanisms underlying these processes remain poorly understood. In previous research, we demonstrated that repressing Cdc24, a guanine nucleotide exchange factor (GEF) for the small GTPases Rac and Cdc42, disrupts fungal cell polarity and impairs hyphal formation in T. rubrum. In this study, we show that Rac deficiency in the Δrac strain minimally affects hyphal formation, as indicated by the cell polarity index (the ratio of a cell's long to short diameter in hyphae). However, simultaneous Rac deficiency and Cdc42 repression in the Δrac/P_ctr4 cdc42 strain significantly disrupted cell polarity, suggesting that Rac and Cdc42 perform overlapping functions in hyphal morphogenesis. Interestingly, Rac deficiency inhibited microconidia formation, whereas cdc42 repression had no detectable impact. Furthermore, adding cysteine, a radical scavenger abundant in keratins, to the growth medium reduced microconidia production in the wild-type strain but not in the Δrac strain. These findings suggest that cysteine in host tissues inhibits Rac-mediated microconidia formation. Overall, this study identifies Rac as a key regulator of T. rubrum morphogenesis, with specific roles in both hyphal development and microconidia formation.