Complete differentiation of the spikes guarantees the final wheat (Triticum aestivum L.) grain yield. A unique wheat mutant that prematurely terminated spike differentiation (ptsd1) was obtained from cultivar Guomai 301 treated with ethyl methane sulfonate (EMS). The molecular mechanism study on ptsd1 showed that the senescence-associated genes (SAGs) were highly expressed, and spike differentiation related homeotic genes were depressed. Cytokinin signal transduction was weakened and ethylene signal transduction was enhanced. The enhanced expression of Ca²⁺ signal transduction related genes and the accumulation of reactive oxygen species (ROS) caused the upper spikelet cell death. Many genes in the WRKY, NAC and ethylene response factor (ERF) transcription factor (TF) families were highly expressed. Senescence related metabolisms, including macromolecule degradation, nutrient recycling, as well as anthocyanin and lignin biosynthesis, were activated. A conserved tae-miR164 and a novel-miR49 and their target genes were extensively involved in the senescence related biological processes in ptsd1. Overall, the abnormal phytohormone homeostasis, enhanced Ca²⁺ signaling and activated senescence related metabolisms led to the spikelet primordia absent their typical meristem characteristics, and ultimately resulted in the phenotype of ptsd1.

Male sterility is a valuable trait for genetic research and production application of wheat (Triticum aestivum L.). NWMS1, a novel typical genic male sterility mutant, was obtained from Shengnong 1, mutagenized with ethyl methane sulfonate (EMS). Microstructure and ultrastructure observations of the anthers and microspores indicated that the pollen abortion of NWMS1 started at the early uninucleate microspore stage. Pollen grain collapse, plasmolysis, and absent starch grains were the three typical characteristics of the abnormal microspores. The anther transcriptomes of NWMS1 and its wild type Shengnong 1 were compared at the early anther development stage, pollen mother cell meiotic stage, and binucleate microspore stage. Several biological pathways clearly involved in abnormal anther development were identified, including protein processing in endoplasmic reticulum, starch and sucrose metabolism, lipid metabolism, and plant hormone signal transduction. There were 20 key genes involved in the abnormal anther development, screened out by weighted gene co-expression network analysis (WGCNA), including SKP1B, BIP5, KCS11, ADH3, BGLU6, and TIFY10B. The results indicated that the defect in starch and sucrose metabolism was the most important factor causing male sterility in NWMS1. Based on the experimental data, a primary molecular regulation model of abnormal anther and pollen developments in mutant NWMS1 was established. These results laid a solid foundation for further research on the molecular mechanism of wheat male sterility.

Chlorophyll biosynthesis must be tightly coupled to light-harvesting chlorophyll a/b-binding protein (LHCP) biogenesis, as free chlorophyll and its precursors are phototoxic. However, precisely how these 2 processes are coordinated in Arabidopsis (Arabidopsis thaliana) remains elusive. Our previous studies demonstrated the role of LHCP TRANSLOCATION DEFECT (LTD) in delivering LHCPs to the chloroplast via the signal recognition particle-dependent pathway. Here, we show that LTD interacts with and stabilizes the chlorophyll biosynthesis enzymes Mg-protoporphyrin methyltransferase and Mg-protoporphyrin monomethylester (MgPME) cyclase, maintaining their activity. We also demonstrate the direct binding of LTD to MgPME, and through crystal structure analysis, we show that the groove of the LTD dimer is critical for MgPME binding. Thus, we propose that LTD transfers MgPME from Mg-protoporphyrin methyltransferase to the MgPME cyclase. These results elucidate a role for LTD in synchronizing chlorophyll biosynthesis with LHCP transport to ensure the correct insertion of chlorophylls into LHCPs.

Tillers not only determine plant architecture but also influence crop yield. To explore the miRNA regulatory network restraining tiller development in a dwarf-monoculm wheat mutant (dmc) derived from Guomai 301 (wild type, WT), we employed miRNome and transcriptome integrative analysis, real-time qRT-PCR, histochemistry, and determinations of the key metabolites and photosynthesis parameters. A total of 91 differentially expressed miRNAs (DEMs) were identified between dmc and WT. Among them, 40 key DEMs targeted 45 differentially expressed genes (DEGs) including the key DEGs encode growth-regulating factors (GRF), auxin response factors (ARF), and other proteins involved in the metabolisms of hormones and carbohydrates, etc. Compared with WT, both the chlorophyll contents and the photosynthesis rate were lower in dmc. The contents of glucose, sucrose, fructose, and maltose were lower in dmc. The contents of auxin (IAA) and zeatin (ZA) were significantly lower, but gibberellin (GA) was significantly higher in the tiller tissues of dmc. This research demonstrated that the DEMs regulating hormone and carbohydrate metabolisms were important causes for dmc to not tiller. A primary miRNA–mRNA regulatory model for dmc tillering was established. The lower photosynthesis rate, insufficient energy, and abnormal hormone metabolisms restrict tillering in dmc.