Abstract
The sessile plants have evolved diverse intrinsic mechanisms to control their proper development under variable environments. In contrast to plastic vegetative development, reproductive traits like floral identity often show phenotypic robustness against environmental variations. However, it remains obscure about the molecular basis of this phenotypic robustness. In this study, we found that eg1 (extra glume1) mutants of rice (Oryza savita L.) showed floral phenotypic variations in different growth locations resulting in a breakdown of floral identity robustness. Physiological and biochemical analyses showed that EG1 encodes a predominantly mitochondria-localized functional lipase and functions in a high temperature-dependent manner. Furthermore, we found that numerous environmentally responsive genes including many floral identity genes are transcriptionally repressed in eg1 mutants and OsMADS1, OsMADS6 and OsG1 genetically act downstream of EG1 to maintain floral robustness. Collectively, our results demonstrate that EG1 promotes floral robustness against temperature fluctuation by safeguarding the expression of floral identify genes through a high temperature-dependent mitochondrial lipid pathway and uncovers a novel mechanistic insight into floral developmental control.
Highlights
The sessile plants have evolved various exquisite adaptive strategies to cope with environmental changes [1,2]
Transcriptomic and genetic analyses revealed that EG1 functions upstream of several floral identity genes, eg, OsMADS1, OsMADS6 and OsG1
We previously found that a rice floral mutant eg1 exhibited a floral variation in different growth conditions [53], implying that EG1 is likely involved in floral robustness
Summary
The sessile plants have evolved various exquisite adaptive strategies to cope with environmental changes [1,2]. A nuclear protein RPL1 (RICE PLASTICITY1) in rice appears to promote the relatively stable plant architecture and panicle structure between different environments [30]. Despite these discoveries, we still know very little about the molecular mechanisms of phenotypic robustness, especially that of plant reproductive traits. Arabidopsis seedlings with decreased cardiolipin in mitochondrial membrane are easier to turn yellow and necrotic under extended darkness or heat due to a failure of mitochondrial morphogenesis, showing a lowered stability [41,44,45] It remains unclear whether mitochondria mediate the phenotypic robustness in plant reproductive organs
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