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Journal of Bacteriology, October 1998, p. 5144-5150, Vol. 180, No. 19
0021-9193/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.

Induction of Ca2+-Calmodulin Signaling by Hard-Surface Contact Primes Colletotrichum gloeosporioides Conidia To Germinate and Form Appressoria

Yeon-Ki Kim, Daoxin Li, and Pappachan E. Kolattukudy*

Departments of Biochemistry and Medical Biochemistry and Neurobiotechnology Center, The Ohio State University, Columbus, Ohio 43210

Received 6 March 1998/Accepted 28 July 1998

Hard-surface contact primes the conidia of Colletotrichum gloeosporioides to respond to plant surface waxes and a fruit-ripening hormone, ethylene, to germinate and form the appressoria required for infection of the host. Our efforts to elucidate the molecular events in the early phase of the hard-surface contact found that EGTA (5 mM) and U73122 (16 nM), an inhibitor of phospholipase C, inhibited (50%) germination and appressorium formation. Measurements of calmodulin (CaM) transcripts with a CaM cDNA we cloned from C. gloeosporioides showed that CaM was induced by hard-surface contact maximally at 2 h and then declined; ethephon enhanced this induction. The CaM antagonist, compound 48/80, completely inhibited conidial germination and appressorium formation at a concentration of 3 µM, implying that CaM is involved in this process. A putative CaM kinase (CaMK) cDNA of C. gloeosporioides was cloned with transcripts from hard-surface-treated conidia. A selective inhibitor of CaMK, KN93 (20 µM), inhibited (50%) germination and appressorium formation, blocked melanization, and caused the formation of abnormal appressoria. Scytalone, an intermediate in melanin synthesis, reversed the inhibition of melanization but did not restore appressorium formation. The phosphorylation of 18- and 43-kDa proteins induced by hard-surface contact and ethephon was inhibited by the treatment with KN93. These results strongly suggest that hard-surface contact induces Ca2+-calmodulin signaling that primes the conidia to respond to host signals by germination and differentiation into appressoria.

* Corresponding author. Mailing address: Departments of Biochemistry and Medical Biochemistry and Neurobiotechnology Center, The Ohio State University, 206 Rightmire Hall, 1060 Carmack Rd., Columbus, OH. Phone: (614) 292-5682. Fax: (614) 292-5379. E-mail: Kolattukudy.2{at}osu.edu.

Journal of Bacteriology, October 1998, p. 5144-5150, Vol. 180, No. 19
0021-9193/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.


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