@article{zhang_xu_zhang_zhong_xing_fan_yan_xu_2024, title={A maize WAK-SnRK1α2-WRKY module regulates nutrient availability to defend against head smut disease}, url={http://dx.doi.org/10.1016/j.molp.2024.09.013}, DOI={10.1016/j.molp.2024.09.013}, abstractNote={Obligate biotrophs depend on living hosts for nutrient acquisition to complete their lifecycle, yet the mechanisms by which hosts restrict nutrient availability to pathogens remain largely unknown. The fungal pathogen Sporisorium reilianum infects maize seedlings and causes head smut disease in inflorescences at maturity, while a cell wall-associated kinase, ZmWAK, provides quantitative resistance against it. Here, we demonstrate that S. reilianum can rapidly activate ZmWAK kinase activity, which is sustained by the 407th Threonine residue in the juxtamembrane domain, enabling it to interact with and phosphorylate ZmSnRK1α2, a conserved sucrose non-fermenting-related kinase α subunit. The activated ZmSnRK1α2 translocates from the cytoplasm to the nucleus, where it phosphorylates and destabilizes the transcription factor ZmWRKY53. The reduced ZmWRKY53 abundance leads to the downregulation of genes involved in transmembrane transport and carbohydrate metabolism, resulting in nutrient starvation for S. reilianum in the apoplast. Our study uncovers a WAK-SnRK1α2-WRKY53 signaling module in maize that conveys phosphorylation cascades from the plasma membrane to the nuclei to confer resistance against head-smut in maize, with profound implications for crop management and application.}, journal={Molecular Plant}, author={Zhang, Qianqian and Xu, Qianya and Zhang, Nan and Zhong, Tao and Xing, Yuexian and Fan, Zhou and Yan, Mingzhu and Xu, Mingliang}, year={2024}, month={Nov} }
 @article{zhu_zhong_xu_guo_zhang_liu_zhang_li_xie_liu_et al._2024, title={The ZmCPK39–ZmDi19–ZmPR10 immune module regulates quantitative resistance to multiple foliar diseases in maize}, url={https://doi.org/10.1038/s41588-024-01968-4}, DOI={10.1038/s41588-024-01968-4}, journal={Nature Genetics}, author={Zhu, Mang and Zhong, Tao and Xu, Ling and Guo, Chenyu and Zhang, Xiaohui and Liu, Yulin and Zhang, Yan and Li, Yancong and Xie, Zhijian and Liu, Tingting and et al.}, year={2024}, month={Nov} }
 @article{zhong_zhu_zhang_zhang_deng_guo_xu_liu_li_bi_et al._2024, title={The ZmWAKL-ZmWIK-ZmBLK1-ZmRBOH4 module provides quantitative resistance to gray leaf spot in maize}, volume={1}, ISSN={["1546-1718"]}, url={https://doi.org/10.1038/s41588-023-01644-z}, DOI={10.1038/s41588-023-01644-z}, abstractNote={AbstractGray leaf spot (GLS), caused by the fungal pathogens Cercospora zeae-maydis and Cercospora zeina, is a major foliar disease of maize worldwide (Zea mays L.). Here we demonstrate that ZmWAKL encoding cell-wall-associated receptor kinase-like protein is the causative gene at the major quantitative disease resistance locus against GLS. The ZmWAKLY protein, encoded by the resistance allele, can self-associate and interact with a leucine-rich repeat immune-related kinase ZmWIK on the plasma membrane. The ZmWAKLY/ZmWIK receptor complex interacts with and phosphorylates the receptor-like cytoplasmic kinase (RLCK) ZmBLK1, which in turn phosphorylates its downstream NADPH oxidase ZmRBOH4. Upon pathogen infection, ZmWAKLY phosphorylation activity is transiently increased, initiating immune signaling from ZmWAKLY, ZmWIK, ZmBLK1 to ZmRBOH4, ultimately triggering a reactive oxygen species burst. Our study thus uncovers the role of the maize ZmWAKL–ZmWIK–ZmBLK1–ZmRBOH4 receptor/signaling/executor module in perceiving the pathogen invasion, transducing immune signals, activating defense responses and conferring increased resistance to GLS.}, journal={NATURE GENETICS}, author={Zhong, Tao and Zhu, Mang and Zhang, Qianqian and Zhang, Yan and Deng, Suining and Guo, Chenyu and Xu, Ling and Liu, Tingting and Li, Yancong and Bi, Yaqi and et al.}, year={2024}, month={Jan} }
 @article{deng_jiang_liu_zhong_liu_liu_liu_yin_sun_xu_2024, title={ZmGDIα-hel counters the RBSDV-induced reduction of active gibberellins to alleviate maize rough dwarf virus disease}, url={https://doi.org/10.1038/s41467-024-51726-7}, DOI={10.1038/s41467-024-51726-7}, abstractNote={Maize rough dwarf disease (MRDD) threatens maize production globally. The P7-1 effector of the rice black-streaked dwarf virus (RBSDV) targets maize Rab GDP dissociation inhibitor alpha (ZmGDIα) to cause MRDD. However, P7-1 has difficulty recruiting a ZmGDIα variant with an alternative helitron-derived exon 10 (ZmGDIα-hel), resulting in recessive resistance. Here, we demonstrate that P7-1 can recruit another maize protein, gibberellin 2-oxidase 13 (ZmGA2ox7.3), which also exhibits tighter binding affinity for ZmGDIα than ZmGDIα-hel. The oligomerization of ZmGA2ox7.3 is vital for its function in converting bioactive gibberellins into inactive forms. Moreover, the enzymatic activity of ZmGA2ox7.3 oligomers increases when forming hetero-oligomers with P7-1/ZmGDIα, but decreases when ZmGDIα-hel replaces ZmGDIα. Viral infection significantly promotes ZmGA2ox7.3 expression and oligomerization in ZmGDIα-containing susceptible maize, resulting in reduced bioactive GA1/GA4 levels. This causes an auxin/cytokinin imbalance and ultimately manifests as MRDD syndrome. Conversely, in resistant maize, ZmGDIα-hel counters these virus-induced changes, thereby mitigating MRDD severity. RBSDV infection increases ZmGA2ox7.3 expression and oligomerization in ZmGDIα-containing maize, leading to reduced bioactive gibberellins and MRDD syndrome. In resistant maize, ZmGDIα-hel attenuates these effects, thereby reducing MRDD severity.}, journal={Nature Communications}, author={Deng, Suining and Jiang, Siqi and Liu, Baoshen and Zhong, Tao and Liu, Qingcai and Liu, Jianju and Liu, Yuanliang and Yin, Can and Sun, Chen and Xu, Mingliang}, year={2024}, month={Aug} }
 @article{zhong_deng_zhu_fan_xu_ye_2023, title={ZmDRR206 functions in maintaining cell wall integrity during maize seedling growth and defense response to external stresses}, url={https://doi.org/10.1016/j.cj.2023.09.007}, DOI={10.1016/j.cj.2023.09.007}, abstractNote={Plants adaptively change their cell wall composition and structure during their growth, development, and interactions with environmental stresses. Dirigent proteins (DIRs) contribute to environmental adaptations by dynamically reorganizing the cell wall and/or by generating defense compounds. A maize DIR, ZmDRR206, was previously reported to play a dominant role in regulation of storage nutrient accumulation in endosperm during maize kernel development. Here we show that ZmDRR206 mediates maize seedling growth and disease resistance by coordinately regulating biosynthesis of cell wall components for cell-wall integrity (CWI) maintenance. Expression of ZmDRR206 was induced in maize seedlings upon pathogen infection. ZmDRR206 overexpression in maize resulted in reduced seedling growth and photosynthetic activity but increased disease resistance and drought tolerance, revealing a tradeoff between growth and defense. Consistently, ZmDRR206 overexpression reduced the contents of primary metabolites and down-regulated genes involved in photosynthesis, while increasing the contents of major cell wall components, defense phytohormones, and defense metabolites, and up-regulated genes involved in defense and cell-wall biosynthesis in seedlings. ZmDRR206-overexpressing seedlings were resistant to cell-wall stress imposed by isoxaben, and ZmDRR206 physically interacted with ZmCesA10, which is a cellulose synthase unit. Our findings suggest a mechanism by which ZmDRR206 coordinately regulates biosynthesis of cell-wall components for CWI maintenance during maize seedling growth, and might be exploited for breeding strong disease resistance in maize.}, journal={The Crop Journal}, author={Zhong, Tao and Deng, Suining and Zhu, Mang and Fan, Xingming and Xu, Mingliang and Ye, Jianrong}, year={2023}, month={Dec} }
 @article{zhu_tong_xu_zhong_2021, title={Genetic dissection of maize disease resistance and its applications in molecular breeding}, url={http://dx.doi.org/10.1007/s11032-021-01219-y}, DOI={10.1007/s11032-021-01219-y}, abstractNote={Abstract Disease resistance is essential for reliable maize production. In a long-term tug-of-war between maize and its pathogenic microbes, naturally occurring resistance genes gradually accumulate and play a key role in protecting maize from various destructive diseases. Recently, significant progress has been made in deciphering the genetic basis of disease resistance in maize. Enhancing disease resistance can now be explored at the molecular level, from marker-assisted selection to genomic selection, transgenesis technique, and genome editing. In view of the continuing accumulation of cloned resistance genes and in-depth understanding of their resistance mechanisms, coupled with rapid progress of biotechnology, it is expected that the large-scale commercial application of molecular breeding of resistant maize varieties will soon become a reality.}, journal={Molecular Breeding}, author={Zhu, Mang and Tong, Lixiu and Xu, Mingliang and Zhong, Tao}, year={2021}, month={May} }
 @article{ye_zhong_zhang_ma_wang_yao_zhang_zhu_xu_2019, title={The Auxin-Regulated Protein ZmAuxRP1 Coordinates the Balance between Root Growth and Stalk Rot Disease Resistance in Maize}, url={http://dx.doi.org/10.1016/j.molp.2018.10.005}, DOI={10.1016/j.molp.2018.10.005}, abstractNote={To optimize fitness, plants must efficiently allocate their resources between growth and defense. Although phytohormone crosstalk has emerged as a major player in balancing growth and defense, the genetic basis by which plants manage this balance remains elusive. We previously identified a quantitative disease-resistance locus, qRfg2, in maize (Zea mays) that protects against the fungal disease Gibberella stalk rot. Here, through map-based cloning, we demonstrate that the causal gene at qRfg2 is ZmAuxRP1, which encodes a plastid stroma-localized auxin-regulated protein. ZmAuxRP1 responded quickly to pathogen challenge with a rapid yet transient reduction in expression that led to arrested root growth but enhanced resistance to Gibberella stalk rot and Fusarium ear rot. ZmAuxRP1 was shown to promote the biosynthesis of indole-3-acetic acid (IAA), while suppressing the formation of benzoxazinoid defense compounds. ZmAuxRP1 presumably acts as a resource regulator modulating indole-3-glycerol phosphate and/or indole flux at the branch point between the IAA and benzoxazinoid biosynthetic pathways. The concerted interplay between IAA and benzoxazinoids can regulate the growth–defense balance in a timely and efficient manner to optimize plant fitness.}, journal={Molecular Plant}, author={Ye, Jianrong and Zhong, Tao and Zhang, Dongfeng and Ma, Chuanyu and Wang, Lina and Yao, Lishan and Zhang, Qianqian and Zhu, Mang and Xu, Mingliang}, year={2019}, month={Mar} }