Mary Beth Mudgett

Honors and Awards

• Chambers Fellow, Stanford University (2011-2014)
• Terman Fellow, Stanford University (2004-2010)
• Teacher of the Year, Associated Students of Stanford University (2008)
• Hellman Faculty Scholar, Stanford University (2005-2006)
• National Research Service Award, National Institute of Health (1997-1999)

Professional Education

Postdoctoral Advisees

Mi Sun Cheong

Graduate & Fellowship Program Affiliations

• Plantbiology

Internet Links

• Mudgett Lab Website

Current Research Interests

My laboratory studies the biochemical mechanisms used by bacterial pathogens to alter plant physiology during infection. Extensive genetic and phenotypic data indicate that the bacterial type three secretion (T3S) system and its protein substrates (referred to as T3S effectors) are the major virulence determinants that promote pathogen colonization in plants. The paradigm for T3S effector function has been that these proteins collectively suppress host defense responses to promote colonization and disease progression. The biological function(s) of most T3S effectors, however, is extremely limited and biochemical support for this paradigm is lacking. Thus, the goal of my research has been to elucidate T3S effector function, identify host targets, and provide fundamental knowledge of how perturbation of host signaling pathways leads to bacterial pathogenesis. To do so, we study the T3S effectors in Xanthomonas campestris pathovar vesicatoria (Xcv), the causal agent of leaf spot disease.

Our research currently focuses on the characterization of three Xcv T3S effectors: XopN, XopD, and AvrBsT. We discovered that these effectors modulate three distinct nodes of defense signal transduction, supporting the paradigm that T3S effectors encode defense suppressors. In addition, our work challenges this paradigm by demonstrating that one effector suppresses disease symptom development, thus illuminating the importance of tolerance promoting factors in bacterial-plant interactions. A few of our important findings include:

• A novel screen to identify new Xanthomonas T3S effector proteins translocated into plant cells during infection.
• Demonstrating that the XopN effector suppresses basal defense and physically interacts with a new tomato receptor kinase associated with basal immunity.
• Demonstrating that the XopD effector is a plant-specific SUMO protease that alters host transcription, promotes pathogen growth, and suppresses host defense responses at the late stages of tissue colonization.
• Identifying new proteins that control phospholipid signaling and disease resistance responses following AvrBsT perturbation.

Publications

• Comparative analysis of the XopD type III secretion (T3S) effector family in plant pathogenic bacteria. Kim JG, Taylor KW, Mudgett MB. Mol Plant Pathol. 2011; 12 (8): 715-30
• Sugar transporters for intercellular exchange and nutrition of pathogens. Chen LQ, Hou BH, Lalonde S, Takanaga H, Hartung ML, Qu XQ, Guo WJ, Kim JG, Underwood W, Chaudhuri B, Chermak D, Antony G, White FF, Somerville SC, Mudgett MB, Frommer WB. Nature. 2010; 468 (7323): 527-32
• SOBER1 phospholipase activity suppresses phosphatidic acid accumulation and plant immunity in response to bacterial effector AvrBsT. Kirik A, Mudgett MB. Proc Natl Acad Sci U S A. 2009; 106 (48): 20532-7
• Xanthomonas T3S Effector XopN Suppresses PAMP-Triggered Immunity and Interacts with a Tomato Atypical Receptor-Like Kinase and TFT1. Kim JG, Li X, Roden JA, Taylor KW, Aakre CD, Su B, Lalonde S, Kirik A, Chen Y, Baranage G, McLane H, Martin GB, Mudgett MB. Plant Cell. 2009; 21 (4): 1305-23
• XopD SUMO protease affects host transcription, promotes pathogen growth, and delays symptom development in xanthomonas-infected tomato leaves. Kim JG, Taylor KW, Hotson A, Keegan M, Schmelz EA, Mudgett MB. Plant Cell. 2008; 20 (7): 1915-29