Skip to main content
ARS Home » Midwest Area » Peoria, Illinois » National Center for Agricultural Utilization Research » Mycotoxin Prevention and Applied Microbiology Research » Research » Publications at this Location » Publication #244946

Title: Allozyme-Specific Modification of a Maize Seed Chitinase by a Protein Secreted by the Fungal Pathogen Stenocarpella maydis

Author
item Naumann, Todd
item Wicklow, Donald

Submitted to: Phytopathology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 2/12/2010
Publication Date: 7/1/2010
Citation: Naumann, T.A., Wicklow, D.T. 2010. Allozyme-Specific Modification of a Maize Seed Chitinase by a Protein Secreted by the Fungal Pathogen Stenocarpella maydis. Phytopathology. 100(7):645-654.

Interpretive Summary: In this research, we discovered that ChitA, a corn defense protein that is present in developing ears, is inactivated by the fungus S. maydis during infection. We also discovered that some breeds of corn have a slightly different ChitA protein that is resistant to this inactivation. S. maydis is one of few fungi that can overcome plant defenses and invade developing ears. Fungal invasion results in corn ear rot, reducing crop yield and contaminating harvested seed with fungal produced toxins. Corn breeders have shown that the ability of different breeds of corn to resist S. maydis ear rot varies. Our results imply that breeds of corn with ChitA that is resistant to inactivation may be more resistant to S. maydis ear rot. This information will help corn breeders develop improved commercial hybrids with better yields and less toxin contamination.

Technical Abstract: Stenocarpella maydis causes both dry-ear rot and stalk rot of maize. Maize inbreds have varying levels of resistance to S. maydis ear rot. The genetic basis of resistance appears to rely on multiple genetic factors, none of which are known. The commonly used stiff stalk inbred B73 has been shown to be strongly susceptible to S. maydis ear rot. Here we report that the ChitA protein alloform from B73, ChitA-F, encoded by a known allele of the chiA gene, is susceptible to modification by a protein secreted by S. maydis (Stm-cmp). We also identify a new allele of chiA (from inbred LH82) which encodes ChitA-S, an alloform of ChitA that is resistant to Stm-cmp modification. Chitinase zymogram analysis of seeds from a commercial field showed the presence of both ChitA alloforms in healthy ears and that ChitA-F, but not ChitA-S, was modified in S. maydis rotted ears. The ChitA-F protein was purified from inbred B73 and ChitA-S from LH82. ChitA-F was modified more efficiently than ChitA-S by S. maydis protein extracts in vitro. The chiA gene from LH82 was cloned and sequenced. It is a novel allele that encodes six polymorphisms relative to the known allele from B73. These findings suggest that the LH82 chiA allele may be a specific genetic determinant that contributes to S. maydis ear rot resistance while the B73 allele may contribute to susceptibility.