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Characterization of Stewart's Wilt Resistance in Juvenile pan1 Mutants of Maize

  • Author(s): Deng, Kaiyue
  • Advisor(s): Smith, Laurie G
  • et al.
No data is associated with this publication.
Abstract

The bacterium Pantoea stewartii subsp. stewartii is the causal agent of Stewart’s Wilt (SW), the most severe bacterial disease that affects sweet corn and maize in north-central and eastern USA. P. stewartii is a vascular pathogen that preferentially colonize the xylem, causing wilting symptoms. Overlapping regions within maize chromosomal bin 1.06 have been identified as multiple disease resistance QTL for both Northern Leaf Blight and Stewart’s Wilt. However, the mechanisms behind the resistance QTL remains unknown. Fine mapping analysis reveals that the pan1 gene, that encodes a leucine-rich repeat receptor-like kinase (LRR-RLK) involved in stomatal complex formation, falls within the QTL. Field-grown adult pan1 mutant plants have been shown to have increased resistance to SW, which indicates that pan1 may underlie the resistance QTL. Our project examines how pan1 increases SW resistance in juvenile maize plants via evaluating SW resistance and quantifying PAN1 protein levels in different maize genotypes. We confirmed that juvenile pan1 mutant plants exhibits consistent resistance phenotype by comparing two independent null pan1 mutants to wild type B73. Our results showed that the stomatal defects in pan1 mutants does not cause the resistance phenotype. Unexpectedly, pan1 mutant allele acts in a dominant manner while PAN1 protein level is reduced by about half of the normal amount in leaf division zone of heterozygous pan1 plants. Our results also indicated that insufficient induction of Type III secretion system does not explain the increased SW resistant phenotype in pan1 mutants. These results will guide further investigation in our effort to elucidate the underlying mechanism of pan1 mutants increased SW resistance.

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This item is under embargo until January 5, 2020.