Summary: Southern corn rust (SCR), caused by Puccinia polysora Underw (P. polysora), is a catastrophic disease affecting maize, leading to significant global yield losses. The disease manifests primarily as pustules on the upper surface of corn leaves, obscuring our understanding of its cellular heterogeneity, the maize's response to its infection and the underlying gene expression regulatory mechanisms. In this study, we dissected the heterogeneity of maize's response to P. polysora infection using single‐cell RNA sequencing. We delineated cell‐type‐specific gene expression alterations in six leaf cell types, creating the inaugural single‐cell atlas of a maize leaf under fungal assault. Crucially, by reconstructing cellular trajectories in susceptible line N110 and resistant line R99 during infection, we identified diverse regulatory programs that fortify R99's resistance across different leaf cell types. This research uncovers an immune‐like state in R99 leaves, characterized by the expression of various fungi‐induced genes in the absence of fungal infection, particularly in guard and epidermal cells. Our findings also highlight the role of the fungi‐induced glycoside hydrolase family 18 chitinase 7 protein (ZmChit7) in conferring resistance to P. polysora. Collectively, our results shed light on the mechanisms of maize resistance to fungal pathogens through comparative single‐cell transcriptomics, offering a valuable resource for pinpointing novel genes that bolster resistance to P. polysora.

Hybrid necrosis, a century-old mystery in wheat, is caused by complementary genes Ne1 and Ne2. Ne2, encoding a nucleotide-binding leucine-rich repeat (NLR) immune receptor, has been cloned, yet Ne1 remains elusive. Here, we report that Ne1, which encodes an alpha/beta hydrolase (ABH) protein generated by structural variation, triggers hybrid necrosis with Ne2 by activating autoimmune responses. We further verify that not only allelic variation but also copy number variation (CNV) of Ne1 are pivotal for hybrid necrosis diversity in wheat. Ne1 likely originates from wild emmer wheat, potentially through duplication and ectopic recombination events. Unlike Ne2, which is frequently selected for rust resistance in wheat breeding, the lower prevalence of Ne1 in modern wheat cultivars is attributed to its association with hybrid necrosis. Altogether, these findings illuminate the co-evolution of the NLR/ABH gene pair in plant development and innate immunity, offering potential benefits for wheat breeding.

As an important food crop worldwide, maize is frequently impacted by drought stress. It is of great significance to study its drought resistance genes and mechanisms, in which DNA methylation modification in the promoter region plays a key role in regulating gene expression and stress resistance. In this study, using PEG6000 and 5-azadC to treat different drought-tolerant maize inbred lines (drought-tolerant R99 and drought-sensitive Mo17), combined with transcriptomic analysis, identified the gene ZmGST2 as being related to drought resistance. Subsequently, the methylation changes in its promoter region were further analyzed. The results indicated that the expression level of ZmGST2 was closely related to the methylation status of its promoter region under drought stress. Specifically, in drought-resistant R99, a decrease in methylation (demethylation) occurred within the CpG island of the ZmGST2 promoter region after drought treatment, which facilitated the expression of this gene and thereby enhanced drought resistance in maize. However, in the drought-sensitive Mo17, this demethylation change did not occur, resulting in reduced drought resistance. Further phenotypic analysis revealed that overexpression of ZmGST2 could enhance the reactive oxygen species scavenging ability in maize roots, improve root growth, and significantly enhance drought resistance. Overall, this study provides both a new candidate gene and a novel approach for molecular breeding aimed at enhancing maize drought resistance.

Southern corn rust (SCR) caused by Puccinia polysora Underw. (P. polysora) poses a serious threat to global maize (Zea mays L.) production. This study used six maize inbred lines (DTMA-45, DTMA-50, R99, N110, P767 and 15B020F3) as materials to systematically explore the response mechanism of maize to southern corn rust through phenotype identification, transcriptome sequencing, functional enrichment analysis, gene co-expression network analysis, and quantitative RT-PCR experiments. Phenotypic analysis shows that DTMA-50, R99 and P767 have strong resistance, while DTMA-45, N110 and 15B020F3 are more sensitive. Transcriptome analysis identified a large number of differentially expressed genes (DEGs), whereas gene ontology (GO) and KEGG (Kyoto Encyclopedia of Genes and Genomes) enrichment analysis showed that these genes are involved in multiple biological processes and metabolic pathways such as defense response, cytoskeleton organization, and plant hormone signaling transduction. Weighted gene co-expression network analysis (WGCNA) identified modules and key genes related to resistance, such as cell wall tissue related genes in the coral2 module and some genes in the ABC transporter and plant pathogen interaction pathways up-regulated in the resistant strain. Quantitative real-time PCR showed that ABCG11 (LOC100281487) and CCR1 (LOC103649447) genes are continuously up-regulated in the early stages of infection in the resistant line R99, which may play an important role in resisting fungal invasion. This study reveals the complex molecular mechanisms underlying maize’s response to southern corn rust, offering important theoretical support and potential targets for maize disease resistance breeding.

Wheat (Triticum aestivum L.) leaf rust [Puccinia triticina (Pt)] causes devastating yield losses globally. Conceivably, breeding and development of cultivars harboring adult plant resistance (APR) to leaf rust (LR) can be an effective way to manage wheat leaf rust. Particularly, mapping of major quantitative trait loci (QTLs) facilitate breeding of LR resistant cultivars. Here, we have mapped QTLs for APR to LR in wheat using wheat population including 215 F_2:3 lines from a Zhoumai 22/Chinese Spring. Bulked segregation analyse (BSA) and simple sequence repeat (SSR) detection of wheat lines digged out the QTLs for APR to LR. Using Manager QTXb20 and Icimapping 3.2 software, some APR QTLs were mapped in Zhoumai 22/Chinese Spring wheat population. Three QTLs of APR to LR detected and designated QLr.zh-2BS, QLr.zh-4BL and QLr.zh-7DS) explained 12.58–13.58%, 7.02–20.22% and 6.73–21.30% of the phenotypic variation, respectively. QLr.zh-4BL and QLr.zh-7DS were derived from Chinese Spring wheat, whereas QLr.zh-2BS emanated from Zhoumai 22. QLr.zh-4BL and QLr.zh-7DS were mapped close to Lr12 and Lr34, respectively, revealling their close link to these loci, correspondingly. Overall, the QTLs related APR to LR, their flanking markers and associated APR genes identified in this study could be useful to genomic resources and marker-assisted select breeding of LR resistance in wheat.