Xiaohong Zhu

Publications (5)31.67 Total impact

• Article: Virus-induced gene silencing offers a functional genomics platform for studying plant cell wall formation.

  Xiaohong Zhu, Sivakumar Pattathil, Koushik Mazumder, Amanda Brehm, Michael G Hahn, S P Dinesh-Kumar, Chandrashekhar P Joshi
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  ABSTRACT: Virus-induced gene silencing (VIGS) is a powerful genetic tool for rapid assessment of plant gene functions in the post-genomic era. Here, we successfully implemented a Tobacco Rattle Virus (TRV)-based VIGS system to study functions of genes involved in either primary or secondary cell wall formation in Nicotiana benthamiana plants. A 3-week post-VIGS time frame is sufficient to observe phenotypic alterations in the anatomical structure of stems and chemical composition of the primary and secondary cell walls. We used cell wall glycan-directed monoclonal antibodies to demonstrate that alteration of cell wall polymer synthesis during the secondary growth phase of VIGS plants has profound effects on the extractability of components from woody stem cell walls. Therefore, TRV-based VIGS together with cell wall component profiling methods provide a high-throughput gene discovery platform for studying plant cell wall formation from a bioenergy perspective.
  Molecular plant 09/2010; 3(5):818-33. · 5.55 Impact Factor
• Article: SGT1 positively regulates the process of plant cell death during both compatible and incompatible plant-pathogen interactions.

  Keri Wang, Srinivasa Rao Uppalapati, Xiaohong Zhu, Savithramma P Dinesh-Kumar, Kirankumar S Mysore
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  ABSTRACT: SGT1 (suppressor of G2 allele of Skp1), an interactor of SCF (Skp1-Cullin-F-box) ubiquitin ligase complexes that mediate protein degradation, plays an important role at both G1-S and G2-M cell cycle transitions in yeast, and is highly conserved throughout eukaryotes. Plant SGT1 is required for both resistance (R) gene-mediated disease resistance and nonhost resistance to certain pathogens. Using virus-induced gene silencing (VIGS) in Nicotiana benthamiana, we demonstrate that SGT1 positively regulates the process of cell death during both host and nonhost interactions with various pathovars of Pseudomonas syringae. Silencing of NbSGT1 in N. benthamiana plants delays the induction of hypersensitive response (HR)-mediated cell death against nonhost pathogens and the development of disease-associated cell death caused by the host pathogen P. syringae pv. tabaci. Our results further demonstrate that NbSGT1 is required for Erwinia carotovora- and Sclerotinia sclerotiorum-induced disease-associated cell death. Overexpression of NbSGT1 in N. benthamiana accelerates the development of HR during R gene-mediated disease resistance and nonhost resistance. Our data also indicate that SGT1 is required for pathogen-induced cell death, but is not always necessary for the restriction of bacterial multiplication in planta. Therefore, we conclude that SGT1 is an essential component affecting the process of cell death during both compatible and incompatible plant-pathogen interactions.
  Molecular Plant Pathology 09/2010; 11(5):597-611. · 3.90 Impact Factor
• Article: Function of endoplasmic reticulum calcium ATPase in innate immunity-mediated programmed cell death.

  Xiaohong Zhu, Jeffrey Caplan, Padmavathi Mamillapalli, Kirk Czymmek, Savithramma P Dinesh-Kumar
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  ABSTRACT: Programmed cell death (PCD) initiated at the pathogen-infected sites during the plant innate immune response is thought to prevent the development of disease. Here, we describe the identification and characterization of an ER-localized type IIB Ca(2+)-ATPase (NbCA1) that function as a regulator of PCD. Silencing of NbCA1 accelerates viral immune receptor N- and fungal-immune receptor Cf9-mediated PCD, as well as non-host pathogen Pseudomonas syringae pv. tomato DC3000 and the general elicitor cryptogein-induced cell death. The accelerated PCD rescues loss-of-resistance phenotype of Rar1, HSP90-silenced plants, but not SGT1-silenced plants. Using a genetically encoded calcium sensor, we show that downregulation of NbCA1 results in the modulation of intracellular calcium signalling in response to cryptogein elicitor. We further show that NbCAM1 and NbrbohB function as downstream calcium decoders in N-immune receptor-mediated PCD. Our results indicate that ER-Ca(2+)-ATPase is a component of the calcium efflux pathway that controls PCD during an innate immune response.
  The EMBO Journal 03/2010; 29(5):1007-18. · 9.20 Impact Factor
• Source

  Available from: appliedbiomics.com

  Article: Induced ER chaperones regulate a receptor-like kinase to mediate antiviral innate immune response in plants.

  Jeffrey L Caplan, Xiaohong Zhu, Padmavathi Mamillapalli, Rajendra Marathe, Radhamani Anandalakshmi, S P Dinesh-Kumar
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  ABSTRACT: Mounting an effective innate immune response against pathogens requires the rapid and global reprogramming of host cellular processes. Here we employed complementary proteomic methods to identify differentially regulated proteins early during a plant's defense response. Besides defense-related proteins, constituents of the largest category of upregulated proteins were cytoplasmic- and ER-residing molecular chaperones. Investigating the significance of upregulated ER chaperones, we find that silencing of ER-resident protein disulfide isomerases NbERp57 and NbP5 and the calreticulins NbCRT2 and NbCRT3 led to partial loss of N immune receptor-mediated defense against Tobacco mosaic virus (TMV). Furthermore, NbCRT2 and NbCRT3 were required for the expression of a previously uncharacterized induced receptor-like kinase (IRK). IRK is a plasma membrane-localized protein required for N-mediated hypersensitive response, programmed cell death, and resistance to TMV. These data support a model in which ER-resident chaperones are required for the accumulation of membrane-bound or secreted proteins during plant innate immunity.
  Cell host & microbe 11/2009; 6(5):457-69. · 13.02 Impact Factor
• Article: Virus-induced gene silencing as a tool to identify host genes affecting viral pathogenicity.

  Xiaohong Zhu, S P Dinesh-Kumar
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  ABSTRACT: Host factors are crucial determinants of viral pathogenicity. Identifying host factors and their contributions to virus infections may lead to the development of novel antiviral strategies. The recently developed virus-induced gene silencing (VIGS) approach offers a rapid means to knock down expression of a given gene in plants. VIGS can be used to determine biological function of candidate genes or to discover new genes that play a role in a given biological pathway. Here, we describe genome-wide Tobacco rattle virus (TRV)-based VIGS screening methods to identify host factors involved in viral pathogenicity.
  Methods in molecular biology (Clifton, N.J.) 02/2008; 451:641-8.