Jia Wen Wu

The FAcilitates Chromatin Transcription (FACT) complex, comprising structure-specific recognition protein 1 (SSRP1) and suppressor of Ty 16 (SPT16), plays a key role in regulating gene transcription by facilitating ATP-independent nucleosome assembly. SSRP1 contains an HMG domain that binds to DNA and regulates cell proliferation, apoptosis, and DNA repair. However, its role in plant development remains poorly understood. In this study, we identified a mutant, small kernel 301 (smk301), characterized by reduced kernel size and semi-dwarfism. Map-based cloning revealed that the mutation affects ZmSSRP1 on chromosome 8, which is expressed throughout maize (Zea mays L.) tissues. ZmSSRP1 localizes to the nucleus and interacts with ZmSPT16 to form the FACT complex. Using RNA-seq and ATAC-seq analyses, we identified 3 candidate target genes involved in hormone pathways, all of which show a significant positive correlation with ZmSSRP1 expression. Notably, ZmSSRP1 was enriched in the chromatin open region of brassinosteroid-deficient dwarf 1 (ZmBRD1), which encodes a Brassinosteroid C-6 Oxidase. This indicates that ZmSSRP1 affects maize development by regulating the transcription of ZmBRD1, thereby influencing the brassinosteroid content in maize. Our findings shed light on how the FACT complex influences maize development by modulating the expression of brassinosteroid-related genes, offering insights into the molecular mechanisms underlying plant growth.

Maize (Zea mays L.) kernel development is a complex and dynamic process involving cell division and differentiation, into a variety of cell types. Epigenetic modifications, including DNA methylation, play a pivotal role in regulating this process. N⁶-methyladenosine modification is a universal and dynamic post-transcriptional epigenetic modification that is involved in the regulation of plant development. However, the role of N⁶-methyladenosine in maize kernel development remains unknown. In this study, we have constructed transcriptome-wide profiles for maize kernels at various stages of early development. Utilizing a combination of MeRIP-seq and RNA-seq analysis, we identified a total of 11,170, 10,973, 11,094, 11,990, 12,203 and 10,893 N⁶-methyladenosine peaks in maize kernels at 0, 2, 4, 6, 8, and 12 days after pollination, respectively. These N⁶-methyladenosine modifications were primarily deposited at the 3’-UTRs and were associated with the conserved motif-UGUACA. Additionally, we found that conserved N⁶-methyladenosine modification are involved in the regulation of genes that are ubiquitously expressed during kernel development. Further analysis revealed that N⁶-methyladenosine peak intensity was negatively correlated with the mRNA abundance of these ubiquitously expressed genes. Meanwhile, we employed phylogenetic analysis to predict potential regulatory proteins involved in maize kernels development and identified several that participate in the regulation of N⁶-methyladenosine modifications. Collectively, our results suggest the existence of a novel post-transcriptional epigenetic modification mechanism involved in the regulation of maize kernels development, thereby providing a novel perspective for maize molecular breeding.

Maize (Zea mays) smut is a common biotrophic fungal disease caused by Ustilago maydis and leads to low maize yield. Maize resistance to U. maydis is a quantitative trait. However, the molecular mechanism underlying the resistance of maize to U. maydis is poorly understood. Here, we reported that a maize mutant caused by a single gene mutation exhibited defects in both fungal resistance and plant development. maize mutant highly susceptible to U. maydis (mmsu) with a dwarf phenotype forms tumors in the ear. A map-based cloning and allelism test demonstrated that one gene encoding a putative arogenate dehydratase/prephenate dehydratase (ADT/PDT) is responsible for the phenotypes of the mmsu and was designated as ZmADT2. Combined transcriptomic and metabolomic analyses revealed that mmsu had substantial differences in multiple metabolic pathways in response to U. maydis infection compared with the wild type. Disruption of ZmADT2 caused damage to the chloroplast ultrastructure and function, metabolic flux redirection, and reduced the amounts of salicylic acid (SA) and lignin, leading to susceptibility to U. maydis and dwarf phenotype. These results suggested that ZmADT2 is required for maintaining metabolic flux, as well as resistance to U. maydis and plant development in maize. Meanwhile, our findings provided insights into the maize response mechanism to U. maydis infection.