Jian-Li Wu

Dr. Jian-Li Wu

orcid

Research Focus & Metrics

Academic Career Length

18Years (2009-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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1 January 2013 in BMC Genomics
Verified
Journal Article
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RNReena Narsai
Reena Narsai
CWChuang Wang
Chuang Wang
JCJie Chen
Jie Chen
JWJian-Li Wu
Jian-Li Wu
Huixia ShouHuixia Shou
Huixia Shou
JWJames Whelan
James Whelan
Every year, substantial crop loss occurs globally, as a result of bacterial, fungal, parasite and viral infections in rice. Here, we present an in-depth investigation of the transcriptomic response to infection with the destructive bacterial pathogen Xanthomonas oryzae pv. oryzae(Xoo) in both resistant and susceptible varieties of Oryza sativa. A comparative analysis to fungal, parasite and viral infection in rice is also presented. Within 24 h of Xoo inoculation, significant reduction of cell wall components and induction of several signalling components, membrane bound receptor kinases and specific WRKY and NAC transcription factors was prominent, providing a framework for how the presence of this pathogen was signalled and response mounted. Extensive comparative analyses of various other pathogen responses, including in response to infection with another bacterium (Xoc), resistant and susceptible parasite infection, fungal, and viral infections, led to a proposed model for the rice biotic stress response. In this way, a conserved induction of calcium signalling functions, and specific WRKY and NAC transcription factors, was identified in response to all biotic stresses. Comparison of these responses to abiotic stress (cold, drought, salt, heat), enabled the identification of unique genes responsive only to bacterial infection, 240 genes responsive to both abiotic and biotic stress, and 135 genes responsive to biotic, but not abiotic stresses. Functional significance of a number of these genes, using genetic inactivation or over-expression, has revealed significant stress-associated phenotypes. While only a few antagonistic responses were observed between biotic and abiotic stresses, e.g. for a number of endochitinases and kinase encoding genes, some of these may be crucial in explaining greater pathogen infection and damage under abiotic stresses. The analyses presented here provides a global view of the responses to multiple stresses, further validates known resistance-associated genes, and highlights new potential target genes, some lineage specific to rice, that play important roles in response to stress, providing a roadmap to develop varieties of rice that are more resistant to multiple biotic and abiotic stresses, as encountered in nature.

1 September 2015 in Journal of Integrative Plant Biology
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QHQi‐Na Huang
Qi‐Na Huang
YSYong‐Feng Shi
Yong‐Feng Shi
XZXiao‐Bo Zhang
Xiao‐Bo Zhang
LSLi‐Xin Song
Li‐Xin Song
BFBao‐Hua Feng
Bao‐Hua Feng
JWJian-Li Wu
Jian-Li Wu
Apremature senescenceand death 128(psd128) mutant was isolated from an ethyl methane sulfonate‐induced rice IR64 mutant bank. The premature senescence phenotype appeared at the six‐leaf stage and the plant died at the early heading stage.psd128exhibited impaired chloroplast development with significantly reduced photosynthetic ability, chlorophyll and carotenoid contents, root vigor, soluble protein content and increased malonaldehyde content. Furthermore, the expression of senescence‐related genes was significantly altered inpsd128. The mutant trait was controlled by a single recessive nuclear gene. Using map‐based strategy, the mutationOryza sativa cell division cycle 48(OsCDC48) was isolated and predicted to encode a putative AAA‐type ATPase with 809 amino‐acid residuals. A single base substitution at position C2347T inpsd128resulted in a premature stop codon. Functional complementation could rescue the mutant phenotype. In addition, RNA interference resulted in the premature senescence and death phenotype.OsCDC48was expressed constitutively in the root, stem, leaf and panicle. Subcellular analysis indicated that OsCDC48:YFP fusion proteins were located both in the cytoplasm and nucleus. OsCDC48 was highly conserved with more than 90% identity in the protein levels among plant species. Our results indicated that the impaired function of OsCDC48 was responsible for the premature senescence and death phenotype.

29 November 2017 in Journal of Integrative Plant Biology
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Journal Article
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XZXiao‐Bo Zhang
Xiao‐Bo Zhang
BFBao‐Hua Feng
Bao‐Hua Feng
HWHui‐Mei Wang
Hui‐Mei Wang
XXXia Xu
Xia Xu
YSYong‐Feng Shi
Yong‐Feng Shi
JWJian-Li Wu
Jian-Li Wu
We previously reported a spotted‐leaf mutant pelota (originally termed HM47) in rice displaying arrested growth and enhanced resistance to multiple races of Xanthomonas oryzae pv. oryzae. Here, we report the map‐based cloning of the causal gene OsPELOTA (originally termed splHM47). We identified a single base substitution from T to A at position 556 in the coding sequence of OsPELOTA, effectively mutating phenylalanine to isoleucine at position 186 in the translated protein sequence. Both functional complementation and over‐expression could rescue the spotted‐leaf phenotype. OsPELOTA, a paralogue to eukaryotic release factor 1 (eRF1), shows high sequence similarity to Drosophila Pelota and also localizes to the endoplasmic reticulum and plasma membrane. OsPELOTA is constitutively expressed in roots, leaves, sheaths, stems, and panicles. Elevated levels of salicylic acid and decreased level of jasmonate were detected in the pelota mutant. RNA‐seq analysis confirmed that genes responding to salicylic acid were upregulated in the mutant. Our results indicate that the rice PELOTA protein is involved in bacterial leaf blight resistance by activating the salicylic acid metabolic pathway.

4 December 2012 in Journal of Integrative Plant Biology
Verified
Journal Article
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BFBao‐Hua Feng
Bao‐Hua Feng
YYYang Yang
Yang Yang
YSYong‐Feng Shi
Yong‐Feng Shi
HSHai‐Chao Shen
Hai‐Chao Shen
HWHui‐Mei Wang
Hui‐Mei Wang
JWJian-Li Wu
Jian-Li Wu
A stable inherited rice spotted‐leaf mutant HM47 derived from an EMS‐induced IR64 mutant bank was identified. The mutant expressed hypersensitive response (HR)‐like symptoms throughout its whole life from the first leaf to the flag leaf, without pathogen invasion. Initiation of the lesions was induced by light under natural summer field conditions. Expression of pathogenesis‐related genes including PAL, PO‐C1, POX22.3 and PBZ1 was enhanced significantly in association with cell death and accumulation of H2O2 at and around the site of lesions in the mutant in contrast to that in the wild‐type (WT). Disease reaction to Xanthomonas oryzae pv. oryzae from the Philippines and China showed that HM47 is a broad‐spectrum disease‐resistant mutant with enhanced resistance to multiple races of bacterial blight pathogens tested. An F2 progeny test showed that bacterial blight resistance to race HB‐17 was co‐segregated with the expression of lesions. Genetic analysis indicated that the spotted‐leaf trait was controlled by a single recessive gene, tentatively named splHM47, flanked by two insertion/deletion markers in a region of approximately 74 kb on the long arm of chromosome 4. Ten open reading frames are predicted, and all of them are expressed proteins. Isolation and validation of the putative genes are currently underway.

13 July 2020 in Plant Physiology
Verified
Journal Article
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YHYan He
Yan He
YSYongfeng Shi
Yongfeng Shi
XZXiaobo Zhang
Xiaobo Zhang
XXXia Xu
Xia Xu
HWHuimei Wang
Huimei Wang
JWJian-Li Wu
Jian-Li Wu
The OsABCI7 transporter interacts with OsHCF222 at thylakoid membranes to regulate reactive oxygen species homeostasis, thereby maintaining thylakoid membrane s

24 August 2019 in Rice
Verified
Journal Article
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ASAtul Prakash Sathe
Atul Prakash Sathe
XSXiaona Su
Xiaona Su
CZchen zheng
chen zheng
TCTing Chen
Ting Chen
XWXiangjing Wei
Xiangjing Wei
JWJian-Li Wu
Jian-Li Wu
Spotted leaf mutants show typical necrotic lesions that appear spontaneously in the absence of any pathogen attack. These mutants are often characterized to exhibit programmed cell death (PCD) and activation of plant defense responses resulting in enhanced disease resistance to multiple pathogens. Here, we reported a novel spotted-leaf mutant, spl40 that showed enhanced disease resistance response. Initially lesions appeared at leaf tips during seedling stage and gradually covered the whole leaf at the tillering stage. The lesion development was light-dependent. spl40 showed obvious cell death at and around the lesion, and burst of reactive oxygen species (ROS) was accompanied by disturbed ROS scavenging system. Photosynthetic capacity was compromised as evidenced by significant reductions in chlorophyll content, important photosynthesis parameters and downregulated expression of photosynthesis-related genes which ultimately led to poor performance of major agronomic traits. spl40 exhibited enhanced resistance to 14 out of 16 races of bacterial blight pathogen of rice, caused by Xanthomonas oryzae pv. oryzae, most probably though activation of SA and JA signaling pathways, owing to upregulated expression of SA and JA signaling genes, though the exact mechanism remain to be elucidated. The spotted-leaf phenotype was controlled by a novel single recessive nuclear gene. Genetic mapping combined with high throughput sequencing analysis identified Os05G0312000 as the most probable candidate gene. Sequencing of ORF revealed a single SNP change from C to T that resulted in non-synonymous change in amino acid residue from leucine to phenylalanine. Interestingly, the complementation plants did not display lesions before heading but showed lesions at the heading stage and the transgenic T1 progenies could be classified into 3 categories based on their lesion intensity, indicating the complex genetic nature of the spl40 mutation. The results obtained here clearly show that genes related to defense and PCD were upregulated in accordance with enhanced disease resistance and occurrence of PCD, whereas the photosynthetic capacity and overall ROS homeostasis was compromised in spl40. Our data suggest that a novel spotted-leaf mutant, spl40, would help to elucidate the mechanism behind lesion development involving programmed cell death and associated defense responses.