Integrative Multi-Omics Analysis Reveals Systemic Transcriptional and Hormonal Reprogramming Associated with a Rice Yellow-Green Leaf Mutant

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.

Authors

Institutions

Publication Details

Journal
Current Issues in Molecular Biology
Published
2026-08-20
DOI
https://doi.org/10.3390/cimb48080848
Primary Topic
Plant Gene Expression Analysis
Type
article
Field-Weighted Citation Impact
0.00

Funders

Controls
|||
ALL TIME
JAN
FEB
MAR
APR
MAY
JUN
JUL
AUG
SEP
OCT
article

Integrative Multi-Omics Analysis Reveals Systemic Transcriptional and Hormonal Reprogramming Associated with a Rice Yellow-Green Leaf Mutant

Xiao Yang, Mangu Hu, Jiawei Liu, Guang Li et al.
Current Issues in Molecular Biology
Plant Gene Expression Analysis
article

Integrative Multi-Omics Analysis Reveals Systemic Transcriptional and Hormonal Reprogramming Associated with a Rice Yellow-Green Leaf Mutant

Xiao Yang, Mangu Hu, Jiawei Liu, Guang Li, Yongxiang Huang
article en

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.

Current Issues in Molecular BiologyVol. 48(8)
South China Agricultural University (CN), Guangdong Ocean University (CN)
Science and Technology Planning Project of Guangdong Province
Openalex Percentile: Top 16%
Plant Gene Expression Analysis
AI Navigator

Ask Laika to Summarize, Analyze, and Connect papers live on the map.

Summarize Papers & Methodologies

Extract key findings, datasets, and comparative methods across publications.

Benchmark Rankings & Visual Analytics

Rank top research institutions, authors, funders, topics, and journals by Field-Weighted Citation Impact (FWCI) and paper volume with instant charts.

Connect Distant Disciplines

Bridge topological clusters on the map to find hidden collaborative intersections.