Plant stomata play a crucial role in photosynthesis by regulating transpiration and gas exchange. Meanwhile, environmental cues can also affect the formation of stomata. Stomatal formation, therefore, is optimized for the survival and growth of the plant despite variable environmental conditions. To adapt to environmental conditions, plants open and close stomatal pores and even regulate the number of stomata that develop on the epidermis. There are great differences in the leaf structure and developmental origin of the cell in the leaf between Arabidopsis and grass plants. These differences affect the fine regulation of stomatal formation due to different plant species. In this paper, a comprehensive overview of stomatal formation and the molecular networks and genetic mechanisms regulating the polar division and cell fate of stomatal progenitor cells in dicotyledonous plants such as Arabidopsis and Poaceae plants such as Oryza sativa and Zea mays is provided. The processes of stomatal formation mediated by plant hormones and environmental factors are summarized, and a model of stomatal formation in plants based on the regulation of multiple signaling pathways is outlined. These results contribute to a better understanding of the mechanisms of stomatal formation and epidermal morphogenesis in plants and provide a valuable theoretical basis and gene resources for improving crop resilience and yield traits.

Stomata are core channels for plant gas exchange and water transpiration, and precise regulation of their development directly impacts photosynthetic efficiency, water use, and stress resistance. Plant receptor kinases, particularly leucine-rich repeat receptor-like kinases (LRR-RLKs), function as key signal sensors: they perceive endogenous and exogenous signals, trigger downstream cascades, and finely regulate stomatal initiation, differentiation, and patterning. Deciphering these mechanisms is therefore critical for improving crop stomatal traits, stress tolerance, and yield. Among receptors regulating stomatal development, LRR-RLKs and leucine-rich repeat receptor-like proteins (LRR-RLPs) are the best studied. Too Many Mouths (TMM), the first identified stomatal receptor (LRR-RLP), forms a multiprotein complex with ERECTA family (ERf) and SERK family LRR-RLKs. This complex recognizes Epidermal Patterning Factors (EPFs)/EPF-like factors (EPFLs) peptides., activates the YODA (YDA)-MAPK cascade, and inhibits the key stomatal lineage transcription factor SPEECHLESS (SPCH), thereby precisely regulating stomatal patterning and differentiation in Arabidopsis . Beyond this core complex, other LRR-RLKs (e.g., HSL1, CLV1, MUS) also regulate Arabidopsis stomatal development or morphogenesis. HSL1 recruits SERK co-receptors and perceives CLE9/10 ligands, but the ligands for CLV1 and MUS in stomatal development remain unknown. Notably, maize PAN1 and PAN2 are essential for asymmetric division of subsidiary mother cells (SMCs) and subsidiary cell (SC) formation, with their cognate ligands also uncharacterized. This review summarizes key advances in stomatal receptor (especially LRR-RLK) mediated stomatal development in Arabidopsis and grasses and highlights core issues such as ligand recognition.

Leaf color mutants are commonly characterized by altered chlorophyll content and aberrant chloroplast development, making them valuable models for investigating photosynthetic mechanisms and chloroplast biogenesis. In this study, an albino mutant was isolated from a population of transgenic maize breeding lines. Genetic analysis indicated that the mutant phenotype is inherited in a Mendelian manner and is controlled by a single nuclear locus. This was supported by a χ² test performed on the T₂ generation, which confirmed a segregation ratio consistent with 3:1 (176:68, χ² = 1.07 < χ²_0.05 = 3.84, p > 0.05). Microscopic examination revealed the absence of normally developed chloroplasts in mutant cells. Further expression analysis of chloroplast genes via Northern blotting and quantitative real-time PCR (qRT-PCR) suggested that the mutation impairs the regulation of plastid-encoded polymerase (PEP)-dependent chloroplast gene expression. Notably, PCR-based co-segregation analysis indicated that the mutant phenotype is associated with the entire inserted vector sequence, rather than a point mutation or a small genomic deletion. In conclusion, this paper reports the isolation and phenotypic characterization of an etiolated mutant from a transgenic maize breeding population, including comparative ultrastructural analysis of chloroplasts, co-segregation validation, and chloroplast gene expression profiling. These results enhance our understanding of the physiological and molecular mechanisms underlying chlorophyll-deficient mutations in plants.

Malic enzyme (ME), a key enzyme involved in various metabolic pathways, catalyzes the oxidative decarboxylation of malate to generate pyruvate, CO₂, and NADPH. This enzyme plays essential roles in plant growth, development, and stress responses. In this study, 13 maize ME genes were identified by performing homologous sequence alignment using the sequences of the Arabidopsis ME gene family as references. Chromosomal localization analysis demonstrated that ME genes were not detected on chromosomes 9 and 10, whereas the remaining eight chromosomes exhibited an uneven distribution of these genes. Phylogenetic analysis indicated a high degree of conservation between maize ME genes and their orthologs in teosinte (Zea luxurians L.) throughout the evolutionary history of Poaceae crops. Furthermore, cis-acting element analysis of promoters demonstrated that members of the maize ME gene family harbor regulatory elements associated with stress responses, phytohormones signaling, and light responsiveness, which suggests their potential role in abiotic stress adaptation. Expression profiling under stress conditions revealed differential expression levels of maize ME genes, with ZmME13 emerging as a promising candidate gene for enhancing stress resistance. These results lay a solid foundation for further investigation into the biological functions of the maize ME gene family.