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.