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Morphological and transcriptional analysis of Colletotrichum lindemuthianum race 7 during early stages of infection in common bean.
Romero, German; González, Sandra; Royero, Wendy; González, Adriana.
Afiliación
  • Romero G; Universidad Nacional de Colombia, Facultad de Ciencias Agrarias, Bogotá, Colombia.
  • González S; Universidad Nacional de Colombia, Instituto de Biotecnología, Bogotá, Colombia.
  • Royero W; Universidad Nacional de Colombia, Instituto de Biotecnología, Bogotá, Colombia.
  • González A; Universidad Nacional de Colombia, Facultad de Ciencias Agrarias, Bogotá, Colombia.
Genet Mol Biol ; 47(1): e20220263, 2024.
Article en En | MEDLINE | ID: mdl-38593425
ABSTRACT
The infection process of the hemibiotrophic fungus Colletotrichum lindemuthianum has been independently studied at the microscopic and genomic levels. However, the relationship between the morphological changes and the pathogenicity mechanisms of the fungus at the early stages of the infection remains uncharacterized. Therefore, this study attempts to bridge this gap by integrating microscopic and transcriptional approaches to understand the infection process of C. lindemuthianum. Fungal structures were followed by fluorescence microscopy for 120 hours. Simultaneously, the transcriptomic profile was made using RNAseq. Morphological characterization shows that appressoria, infective vesicles, and secondary hypha formation occur before 72 hours. Additionally, we assembled 38,206 transcripts with lengths between 201 and 3,548 bp. The secretome annotation revealed the expression of 1,204 CAZymes, of which 17 exhibited secretion domains and were identified as chitinases and ß-1,3-glucanases, 27 were effector candidates, and 30 were transport proteins mostly associated with ABC-type. Finally, we confirmed the presence and expression of CAC1 role during the appressoria formation of Clr7. This result represents the first report of adenylate cyclase expression evaluated under three different approaches. In conclusion, C. lindemuthianum colonizes the host through different infection structures complemented with the expression of multiple enzymes, where CAC1 favors disease development.