Jingyi  Wang Wang

Dr. Jingyi Wang Wang


Research Focus & Metrics

Academic Career Length

3Years (2024-Present)

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

Representative Publications

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雅侍雅琼 侍
雅琼 侍
ZJZihao Jin
Zihao Jin
JWJingyi Wang Wang
Jingyi Wang Wang
GZGuangkuo Zhou
Guangkuo Zhou
FWFang Wang
Fang Wang
YPYunling Peng
Yunling Peng
Drought stress seriously affects the growth, development, yield, and quality of maize. This study aimed to investigate the effects of exogenous 5-ALA on root morphology and physiological changes in maize seedlings and to detect its regulatory network. The results showed that adding 25 mg/L 5-ALA accelerated root morphogenesis (root average diameter, main root length, total root length, and root surface area) and promoted dry matter accumulation and free radical removal. Transcriptome analysis showed that after applying exogenous 5-ALA, differently expressed genes (DEGs) were mainly involved in histidine metabolism, amino acid biosynthesis, plasma membrane components, secondary active sulfate transmembrane transporter activity, and anion reverse transporter activity. Two inbred lines specifically responded to organelle and structural molecular activity, and 5-ALA may regulate maize roots to achieve drought tolerance through these two pathways. In addition, candidate genes that may regulate maize root growth were screened by weighted gene co-expression network analysis (WGCNA). These genes may play important roles in alleviating drought stress through lignin synthesis, heat shock proteins, iron storage and transport, calcium binding proteins, and plasma membrane regulation of exogenous regulator 5-ALA. Our results may provide a theoretical basis for clarifying the response of maize seedling roots to drought and the mechanism of exogenous hormones in alleviating drought.

27 May 2025 in Preprints.org
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JWJingyi Wang Wang
Jingyi Wang Wang
TWTing Wang
Ting Wang
YSYaqiong Shi
Yaqiong Shi
FWFang Wang
Fang Wang
YPYunling Peng
Yunling Peng
Jasmonic acid (JA) plays a crucial role in plant disease resistance defense. To explore its regulatory mechanism in plant resistance to pathogens, this study focused on Ustilago maydis (U. maydis) using, exogenous application of different concentrations of JA and jasmonic acid inhibitor ibuprofen (IBU), combined with physiological and biochemical analysis, cytological observation, transcriptome analysis and weighted gene co-expression network analysis (WGCNA), to systematically analyze the JA-induced disease resistance mechanism in maize. The results showed that 0.1 mmol/L JA treatment significantly inhibited pathogen mycelial growth (with an inhibition rate of 19.0%) and improved plant disease resistance (disease index decreased by 52.65%), while IBU treatment exacerbated disease susceptibility. Physiological and biochemical analysis showed that JA treatment significantly increased the activity of defense enzymes (POD, PPO, β-1,3-GA), reduced malondialdehyde (MDA) content and alleviated membrane damage. Cytological observation demonstrated that JA maintained the integrity of mesophyll cells and vascular bundle sheath structures, effectively inhibiting cell expansion and division caused by pathogens. Transcriptome analysis indicated that JA induced more differentially expressed genes (DEGs) in the susceptible variety Ye478 compared to the resistant variety Qi319, and these genes were significantly enriched in phenylpropanoid biosynthesis, starch and sucrose metabolism pathways. Through WGCNA analysis, 16 key genes were identified from four modules, further identifying six candidate genes related to disease resistance, including self-resistance-resistant genes (PP2C, WRKY) and JA-induced resistance-related genes (CGT, GLCAT, RING zinc finger protein, CaM). In summary, JA significantly enhances maize resistance to U. maydis by enhancing defense enzyme activity, maintaining cell structure stability and regulating key gene expression. This study provides an important theoretical basis for clarifying the JA-mediated disease resistance mechanism and disease-resistant breeding.