## 3 Discussion
PcTbcc1 directly regulates vegetative development and assumes new roles in the pathophysiological development of _P. capsici_. In addition, the promotion of growth, microtubules, and tubulin-folding cofactor-dependent processes (including intracellular and vesicular transport) facilitates the transport of cargoes, virulent determinants (secreted proteins/effector proteins), and the relay of internal cues necessary to drive pathogenic differentiation in invading pathogens during pathogen interactions. For instance, the targeted disruption of microtubule-associated dynein motor protein in rice blast pathogen abolished conidiation and rendered the _\(\Delta Modync1I2\)_ strains non-pathogenic [27]. Similarly, we demonstrated that the deletion of _PcTBCC1_ significantly suppressed asexual sporulation, delayed encystment, compromised zoospore survival, and attenuated the virulence of _P. capsici_. In addition, pathogenic microbes that cause diseases in seasonal crops experience a window of over-wintering/over-summering periods, often associated with nutrient limitation and multiple harsh conditions. Most phytopathogenic microbes have evolved diverse survival strategies (by going into either total or partial hibernation) to drastically reduce the rate of metabolism and other energy-intensive physiological developmental processes, including vegetative growth [28]. The current study showed that the targeted disruption of _PcTBCC1_ caused a significant increase in the vegetative growth of _PcTBCC1_ gene-defective strains under nutrient-deficient conditions. Meanwhile, the vegetative growth of \(\Delta\)_Pctbcc1_ strains was indistinguishable from the wild-type strains under nutrient-sufficient conditions. These observations suggest that PcTbcc1 mediates the economic utilization of nutrients to ensure the survival of _P. capsici_ under starvation- or stress-proneconditions by acting directly or indirectly to minimize vegetative morphogenesis and the rate of metabolic processes. These observations are in tandem with the fundamental knowledge that fungi and oomycetes generally switch from the vegetative growth phase to asexual sporulation (i.e., the reproductive phase) in response to nutrient limitations [29; 30]. Coupled with the significant reductions observed in sporulation characteristics of the \(\Delta\)_PcTbcc1_ strains, there is adequate support for the reasoning that PcTbcc1 functions as a nutrient-sensitive genetic switch that promotes asexual sporulation by suppressing morphological differentiation to support the survival of _P. capsaicin_ under nutrient harsh conditions and facilitating the mobilization of nutrients from the host plant by enhancing the virulence of _P. capsaicin_ (Figure 7). Microtubules and tubulins are crucial targets of diverse fungicides [31; 32]. However, the direct contribution of microtubules, tubulins, and tubulin-folding cofactors to the pathophysiological development of oomycetes remains unknown. Understanding the regulatory parameters of pathogenesis in this pathogen is of great concern to the broader scientific community because it poses a substantial economic burden. Findings from the current investigations underscore the crucial contributions of PcTbcc1, a novel TBCC domain-containing hypothetical protein, to the sporogenesis and virulence of _P. capsaicin_. These findings provide theoretical and practical insights that will facilitate the deployment of PcTbcc-1 and likely other tubulin-folding cofactors in _P. capsaicin_ as targets for developing oomycetes to control the Phytophthoranora blight pathogen.