Aug 2026· Current Issues in Molecular Biology· Vol 48, pp. 848· 0 citations· 48 references
Medicine
TL;DR
Yel, a stably inherited rice mutant with a dwarf and yellow-green leaf phenotype controlled by a single recessive nuclear gene, is identified and it is proposed that the yel phenotype is associated with a self-reinforcing inhibitory loop of “passive synthesis inhibition” and “active degradation acceleration".
Abstract
Leaf-color mutants are crucial for elucidating chlorophyll metabolism mechanisms. Here, we identified yel, a stably inherited rice mutant with a dwarf and yellow-green leaf phenotype controlled by a single recessive nuclear gene. Using BSA-seq, we mapped the candidate causal gene to OsMPEC, encoding a magnesium protoporphyrin IX monomethyl ester cyclase with a G→T substitution. Multi-omics analysis revealed that the functional deficiency of OsMPEC protein—despite unchanged transcript levels—triggers global transcriptional repression of the chlorophyll metabolic network. This defect caused distinct metabolic consequences: impaired synthesis at the early stage (yel1) and toxic metabolite accumulation at the later stage (yel2). Furthermore, metabolic collapse induced systemic reprogramming of hormone signaling, shifting from pro-growth to stress and senescence modes. We propose that the yel phenotype is associated with a self-reinforcing inhibitory loop of “passive synthesis inhibition” and “active degradation acceleration.” This study clarifies OsMPEC’s role in chlorophyll homeostasis and demonstrates how a single genetic defect drives phenotype- through to network-level cascading effects.
Findings establish HY5 as a critical coordinator of metabolic and defence networks, providing mechanistic insight into how light-responsive transcriptional regulation shapes plant stress resilience and offering targets for engineering stress-tolerant crops.
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