November
1998
, Volume
11
, Number
11
Pages
1,110
-
1,118
Authors
Carl
Simmons
,
1
Sabine
Hantke
,
1
Susan
Grant
,
1
Gurmukh S.
Johal
,
2
and
Steven P.
Briggs
1
Affiliations
1Pioneer Hi-Bred International, Inc., 7300 N.W. 62nd Avenue, Johnston, IA 50131, U.S.A.; 2Department of Agronomy, University of Missouri, Columbia 65211, U.S.A.
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RelatedArticle
Accepted 14 July 1998.
Abstract
The maize lethal leaf spot 1 (lls1) mutant exhibits enhanced resistance to fungal pathogens. The lls1 resistance to Cochliobolus heterostrophus has two components: (i) lesion number is reduced 40% relative to wild type; and (ii) the lesions that do form often do not contain viable fungus. This lesion sterility is dependent upon leaf maturity and light, whereas reduced lesion number is not. The lls1 lesions express pathogenesis-related proteins at high levels, so lesion sterility likely results from activation of defense systems and necrosis. Reduced lesion number is correlated with a reduction of C. heterostrophus spore germination, hyphal growth, and haustoria formation on the leaf epidermis. The rust pathogen Puccinia sorghi has reduced pustule formation on lls1, and its germination and growth are also slowed on the epidermis. However, after entering the mesophyll through stomata, P. sorghi can form pustules on lls1, and even green islands within necrotic lls1 lesions. In situ mRNA hybridization shows that Lls1 is predominantly expressed in the leaf epidermis, coincident with the site of resistance in the mutant.
JnArticleKeywords
Additional keywords:
chitinase,
Cochliobolus carbonum,
Colletotrichum graminicola,
PR1.
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ArticleCopyright
© 1998 The American Phytopathological Society