TBCC Domain-Containing Protein Regulates Sporulation and Virulence of Phytophthora capsici via Nutrient-Responsive Signaling
Phytopathogenic oomycetes, particularly , the causal agent of Phytophthora blight disease in essential vegetables and fruit crops, remains a persistent challenge in the vegetable production industry. However, the core molecular regulators of the pathophysiology and broad-range host characteristics o...
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Veröffentlicht in: | International journal of molecular sciences 2024-11, Vol.25 (22), p.12301 |
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Hauptverfasser: | , , , , , , , , , , |
Format: | Artikel |
Sprache: | eng |
Schlagworte: | |
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Zusammenfassung: | Phytopathogenic oomycetes, particularly
, the causal agent of Phytophthora blight disease in essential vegetables and fruit crops, remains a persistent challenge in the vegetable production industry. However, the core molecular regulators of the pathophysiology and broad-range host characteristics of
remain unknown. Here, we used transcriptomics and CRISPR-Cas9 technology to functionally characterize the contributions of a novel gene (
) coding for a hypothetical protein with a tubulin-binding cofactor C domain with a putative chloroplast-targeting peptide (cTP) to the pathophysiological development of
. We observed significant upregulation in the expression of
during pathogen-host interactions. However, the vegetative growth of the ∆
strains was not significantly different from the wild-type strains.
gene replacement significantly compromised the sporulation, pathogenic differentiation, and virulence of
. At the same time, ∆
strains were sensitive to cell wall stress-inducing osmolytes. These observations, coupled with the close evolutionary ties between
and pathogenic oomycetes and algae, partly support the notion that
is a conserved determinant of pathogenesis. This study provides insights into the significance of tubulin-binding cofactors in
and underscores the potential of PcTbcc1 as a durable target for developing anti-oomycides to control phytopathogenic oomycetes. |
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ISSN: | 1422-0067 1661-6596 1422-0067 |
DOI: | 10.3390/ijms252212301 |