Lectin receptor-like kinase LecRK-VIII.2 is a missing link in MAPK signaling-mediated yield control.
Wenjun XiaoShuai HuXiaoxiao ZouRuqiong CaiRui LiaoXiaoxia LinRuifeng YaoXinhong GuoPublished in: Plant physiology (2022)
The energy allocation for vegetative and reproductive growth is regulated by developmental signals and environmental cues, which subsequently affects seed output. However, the molecular mechanism underlying how plants coordinate yield-related traits to control yield in changing source-sink relationships remains largely unknown. Here, we discovered the lectin receptor-like kinase LecRK-VIII.2 as a specific receptor-like kinase that coordinates silique number, seed size, and seed number to determine seed yield in Arabidopsis (Arabidopsis thaliana). The lecrk-VIII.2 mutants develop smaller seeds, but more siliques and seeds, leading to increased yield. In contrast, the plants overexpressing LecRK-VIII.2 form bigger seeds, but less siliques and seeds, which results in similar yield to that of wild-type plants. Interestingly, LecRK-VIII.2 promotes the growth of the rosette, root, and stem by coordinating the source-sink relationship. Additionally, LecRK-VIII.2 positively regulates cell expansion and proliferation in the seed coat, and maternally controls seed size. The genetic and biochemical analyses demonstrated that LecRK-VIII.2 acts upstream of the mitogen-activated protein kinase (MAPK) gene MPK6 to regulate silique number, seed size, and seed number. Collectively, these findings uncover LecRK-VIII.2 as an upstream component of the MAPK signaling pathway to control yield-related traits and suggest its potential for crop improvement aimed at developing plants with stable yield, a robust root system, and improved lodging resistance.
Keyphrases
- signaling pathway
- genome wide
- oxidative stress
- wild type
- arabidopsis thaliana
- tyrosine kinase
- protein kinase
- magnetic resonance
- epithelial mesenchymal transition
- gene expression
- climate change
- dna methylation
- magnetic resonance imaging
- copy number
- bone marrow
- cell therapy
- induced apoptosis
- transcription factor
- human health