H
Hongge Jia
Researcher at University of Florida
Publications - 27
Citations - 2300
Hongge Jia is an academic researcher from University of Florida. The author has contributed to research in topics: Xanthomonas citri & Canker. The author has an hindex of 16, co-authored 25 publications receiving 1768 citations. Previous affiliations of Hongge Jia include Chinese Academy of Sciences & University of Kentucky.
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Journal ArticleDOI
Targeted genome editing of sweet orange using Cas9/sgRNA.
Hongge Jia,Nian Wang +1 more
TL;DR: This is the first report of targeted genome modification in citrus using the Cas9/sgRNA system, a system that holds significant promise for the study of citrus gene function and for targeted genetic modification.
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Genome editing of the disease susceptibility gene CsLOB1 in citrus confers resistance to citrus canker.
TL;DR: This study indicates that genome editing using CRISPR technology will provide a promising pathway to generate disease‐resistant citrus varieties.
Journal ArticleDOI
Lateral organ boundaries 1 is a disease susceptibility gene for citrus bacterial canker disease
Yang Hu,Junli Zhang,Hongge Jia,Davide Sosso,Ting Li,Wolf-Bernd Frommer,Bing Yang,Frank F. White,Nian Wang,Jeffrey B. Jones +9 more
TL;DR: The results indicate that CBC-inciting species of Xanthomonas exploit a single host disease susceptibility gene by altering the expression of an otherwise developmentally regulated gene using any one of a diverse set of TAL effector genes in the pathogen populations.
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Modification of the PthA4 effector binding elements in Type I CsLOB1 promoter using Cas9/sgRNA to produce transgenic Duncan grapefruit alleviating XccΔpthA4:dCsLOB1.3 infection
TL;DR: The data suggest that activation of a single allele of susceptibility gene CsLOB1 by PthA4 is sufficient to induce citrus canker disease, and mutation in the promoters of both alleles of CslOB1 is probably required to generate canker-resistant plants.
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Nuclear localization sequence of FUS and induction of stress granules by ALS mutants
TL;DR: The results suggest that the ALS mutations in FUS NLS can impair FUS nuclear localization, induce cytoplasmic inclusions and stress granules, and potentially perturb RNA metabolism.