Small GTPase Rac promotes hyphal formation and microconidiogenesis in <i>Trichophyton rubrum</i>

Morphogenesis plays a pivotal role in the infection process of <i>Trichophyton rubrum</i>, a primary aetiological agent of dermatophytosis that inhabits superficial human tissues. <i>T. rubrum</i> proliferates by extending filamentous structures, or hyphae, which are composed of highly polarized cells. In response to environmental stimuli, <i>T. rubrum</i> also produces asexual spores called microconidia, consisting of individual cells. Although these dynamic morphological changes are critical for <i>T. rubrum</i> 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 <i>T. rubrum</i>. In this study, we show that Rac deficiency in the Δ<i>rac</i> 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 Δ<i>rac</i>/P_<i>ctr4</i> <i>cdc42</i> strain significantly disrupted cell polarity, suggesting that Rac and Cdc42 perform overlapping functions in hyphal morphogenesis. Interestingly, Rac deficiency inhibited microconidia formation, whereas <i>cdc42</i> 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 Δ<i>rac</i> strain. These findings suggest that cysteine in host tissues inhibits Rac-mediated microconidia formation. Overall, this study identifies Rac as a key regulator of <i>T. rubrum</i> morphogenesis, with specific roles in both hyphal development and microconidia formation.