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NLSS3 Impairs SHM1 Autophagic Degradation to Regulate Leaf Morphology and Salt Tolerance in Rice
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The inherent trade-off between optimal plant architecture and robust stress resilience represents a fundamental challenge in the breeding of high-yielding rice cultivars. Overcoming this antagonistic relationship requires identifying master regulatory genes that can coordinately modulate both growth and stress response pathways. In this study, NLSS3 (Narrow Leaf and Salt Sensitive 3) was identified as a pleiotropic regulator governing both leaf morphogenesis and salinity tolerance in rice. NLSS3 physically interacts with SHM1 (serine hydroxymethyltransferase), protecting it from autophagy-mediated degradation and thereby enhancing its protein stability. The loss of NLSS3 function causes SHM1 depletion, resulting in serine deficiency and heightened salt sensitivity. Strikingly, SHM1 overexpression not only restored leaf width in the nlss3 mutant but also significantly increased grain yield and salt tolerance in wild-type plants. Moreover, the superior NLSS3 haplotype Hap1, which is predominant in japonica accessions, shows high expression and enhanced salinity tolerance. These findings establish NLSS3 as a central "autophagy guardian" that integrates plant development and environmental adaptation through the regulation of protein homeostasis. This work positions NLSS3 as a promising target for precision breeding to engineer high-yielding and stress-resilient rice varieties.
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