Functions of Leucine Rich Repeat Receptor-Like Kinases (LRR-RLKs) in Arabidopsis Sexual Reproduction
- Author(s): Khamsuk, Ornusa
- Advisor(s): Yang, Zhenbiao
- et al.
Sexual reproduction is a critical process in life cycle of flowering plants. To achieve successful reproduction, some important steps are required including gametogenesis, pollination and fertilization. Gametogenesis refers to the development of haploid gametes (egg and sperm). Pollination requires pollen-pistil recognition to promote pollen tube growth toward the ovule. During fertilization, the reproductive gametes fuse to each other and embryo is produced. In this study, different approaches were used to clarify the biological function of three leucin rich repeat receptor-like kinases (LRR-RLKs); RLK B, RLK C and RLK D, during sexual reproduction in Arabidopsis. RLK B, RLK C and RLK D belong to LRR VI, LRR III and LRR VIII-type of the LRR-RLK subfamily, respectively. According to the phenotypic characterization of different combination of mutants, we show that RLK C function redundantly with RLK B and RLK D to regulate male and female fertilities. In rlk c, the synergids were not specified in some embryo sacs resulted in an increase of unfertilized ovules. Mutations in RLK B and RLK D could enhance phenotypes of rlk c. The rlk c rlk b plant exhibited severe defect in pollen tube guidance and seed production. It is most likely that RLK C and RLK B function redundantly to elicit a signal transduction pathway involved in synergid specification or female gametophyte development. By contrast, rlk c rlk d-2 caused more severe defect in pollen fertility. In both cases, the major contribution for gamete fertility is from RLK C signaling due to no apparent phenotype in the rlk b and rlk d single mutants. In addition, the rlk b rlk d-2 mutant did not show phenotype, indicating their unique functions in reproduction. According to dominant-negative (DN) study, the LAT52p::DN-RLK C receptor lacking the kinase domain enhanced a defect in male fertility in the rlk c mutant. This confirms that the functional redundancy in RLK C is essential to regulate male fertility. Taken together, we provide evidence that RLK C, RLK B and RLK D function to achieve fully fertility of the reproductive gametes.