Two novel genes induced by ward-surface contact of Colletotrichum gloeosporioides conidia

Citation
Yk. Kim et al., Two novel genes induced by ward-surface contact of Colletotrichum gloeosporioides conidia, J BACT, 182(17), 2000, pp. 4688-4695
Citations number
50
Categorie Soggetti
Microbiology
Journal title
JOURNAL OF BACTERIOLOGY
ISSN journal
00219193 → ACNP
Volume
182
Issue
17
Year of publication
2000
Pages
4688 - 4695
Database
ISI
SICI code
0021-9193(200009)182:17<4688:TNGIBW>2.0.ZU;2-9
Abstract
Germinating conidia of many phytopathogenic fungi must differentiate into a n infection structure called the appressorium in order to penetrate into th eir hosts. This differentiation is known to require contact with a hard sur face. However, the molecular basis for this requirement is not known. Induc tion of this differentiation in the avocado pathogen, Colletotrichum gloeos porioides, by chemical signals such as the host's surface wax or the fruit- ripening hormone, ethylene, requires contact of the conidia with a hard sur face for about 2 h, To study molecular events triggered by hard-surface con tact, we isolated several genes expressed during the early stage of hard-su rface treatment by a differential-display method. The genes that encode Col letotrichum hard-surface induced proteins are designated chip genes. In thi s study, we report the characterization of CHIP2 and CHIP3 genes that would encode proteins with molecular masses of 65 and 64 kDa, respectively, that have no homology to any known proteins. The CHIP2 product would contain a putative nuclear localization signal, a leucine zipper motif, and a heptad repeat region which might dimerize into coiled-coil structure. The CHIP3 pr oduct would be a nine-transmembrane-domain-containing protein. RNA blots sh owed that CHIP2 and CHIP3 are induced by a 2-h hard-surface contact. Howeve r, disruption of these genes did not affect the appressorium-forming abilit y and did not cause a significant decrease in virulence on avocado or tomat o fruits suggesting that C. gloeosporioides might have genes functionally r edundant to CHIP2 and CHIP3 or that these genes induced by hard-surface con tact control processes not directly involved in pathogenesis.