Meiosis, a critical process for sexual reproduction, requires precise regulation to ensure the correct progression of meiotic stages. In yeast and animals, errors in meiotic recombination and homologous chromosomes synapsis bring a surveillance mechanism named pachytene checkpoint to prevent pachytene exit. However, most plant mutants with defects in meiotic prophase Ⅰ continue cell cycle progression, which hindered the characterization of factors controlling the prophase Ⅰ to metaphase Ⅰ transition. Here, we characterized a male-sterile mutant in maize, prolonged prophase1 (pp1), which exhibited pachytene and diakinesis arrest in male meiosis, and abnormal chromatin condensation. Using map-based cloning, the PP1 gene was isolated as a PHD family transcription factor, and its transcripts of PP1 were preferentially accumulated in tapetum and male germline cells during microsporogenesis. Transcriptomic analysis of the pp1 mutant revealed downregulation of genes associated with chromatin assembly, cell cycle, and male meiosis, correlating with observed meiotic arrest and chromatin condensation defects. These findings highlight the role of PP1 in maize microsporogenesis, and providing more insights into the mechanisms regulating the meiotic progression in maize.

Grain protein content (GPC) is an indicator of cereal nutritional quality. Identification of genes involved in the regulation of GPC provides targets for molecular breeding for crop protein quality. We characterized a maize gene encoding the putative amino acid transporter ZmAAP6, a gene expressed mainly in immature seeds, especially in the basal endosperm transfer layer. Total protein and zein contents were decreased in ZmAAP6 null mutants and increased in ZmAAP6 overexpression (OE) lines, consistent with their changed in the size of protein bodies. Metabolic and transcriptomic analysis supported the regulatory role of ZmAAP6 in amino acid transportation. These results suggest that ZmAAP6 functions as a positive regulator of GPC in maize, shedding new light on the genetic basis of GPC regulation.