| Summary: | Leaf morphology is a crucial aspect of plant architecture, yet the molecular mechanisms underlying leaf development remain incompletely understood. In this study, a narrow leaf mutant, <i>m625,</i> was identified in rice (<i>Oryza sativa</i> L.), exhibiting pleiotropic developmental defects. Pigment measurement revealed reduced levels of photochromic pigments in <i>m625</i>. Cytological analysis demonstrated that the <i>m625</i> gene affected vascular patterns and cell division. Specifically, the narrowing of the leaf was attributed to a decrease in small vein number, shorter vein spacing, and an abnormal V-shaped arrangement of bulliform cells, while the thickening was caused by longer leaf veins, thicker mesophyll cells, and an increased number of parenchyma cell layers. The dwarf stature and thickened internode were primarily due to shortened internodes and an increase in cell layers, respectively. Positional cloning and complementation assays indicated that the <i>m625</i> gene is a novel allele of <i>NAL1</i>. In the <i>m625</i> mutant, a nucleotide deletion at position 1103 in the coding sequence of <i>NAL1</i> led to premature termination of protein translation. Further RNA-Seq and qRT-PCR analyses revealed that the <i>m625</i> gene significantly impacted regulatory pathways related to IAA and ABA signal transduction, photosynthesis, and lignin biosynthesis. Moreover, the <i>m625</i> mutant displayed thinner sclerenchyma and cell walls in both the leaf and stem, particularly showing reduced lignified cell walls in the midrib of the leaf. In conclusion, our study suggests that <i>NAL1</i>, in addition to its known roles in IAA transport and leaf photosynthesis, may also participate in ABA signal transduction, as well as regulate secondary cell wall formation and sclerenchyma thickness through lignification.
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