侧根对植物根系形态结构的形成及功能起着至关重要的作用。已知内外因子均可影响侧根的发育，但调控机制知之甚少。申请人团队发现一个LRR-RLK，RLK68，在侧根中特异表达，缺失突变体rlk68的侧根没有明显缺陷型表型，RLK68及同源基因RLK165组成的双缺失突变体rlk68 rlk165表现出显著的侧根减少表型。遗传互补实验证明该表型的确由这两个RLKs缺失造成的。RLK68在主、侧根中均表现出典型的极性分布，与PIN1相似。另外，双突变体根的生长对多肽激素CEP5表现出超敏感表型，预示RLK68及RLK165可能在CEP-CEPR途径中起负调控作用。本项目旨在研究RLK68及RLK165与PIN1、CEP-CEPR途径的关系，并阐明这两个RLKs调控侧根发育的详细信号转导途径。除此之外，本项目将从表达图谱出发，通过遗传学手段找到更多的参与侧根发育的其他LRR-RLKs。

Lateral roots play key roles in determining the architecture and functions of a plant root system. It has been known that internal factors and external cues are both critical in regulating lateral root primordium initiation and development. Yet the related molecular mechanisms are poorly understood. We have generated the promoter::GUS transgenic plants for all 223 leucine-rich repeat receptor-like protein kinases (LRR-RLKs) in Arabidopsis. Our detailed analyses indicated that one of these LRR-RLKs, RLK68, exhibits a lateral root primordium specific expression pattern. A single loss-of-function mutant, rlk68, does not show any lateral root defects. Double mutant generated from the alleles of RLK68 and its closest paralog, RLK165, displays a significantly reduced lateral root phenotype. Genetic complementation analysis demonstrated that the lateral root defects are solely cause by the lesions of both RLKs. Interestingly, subcellular localization analysis indicated that RLK68 localizes at the bottom side of primary and lateral root cells, similar to that of a PIN1 protein. In addition, the roots of the rlk68 rlk165 double mutant are hypersensitive to the treatment of CEP5, a peptide hormone known to regulate primary and lateral root growth and development. The fact that rlk68 rlk165 shows an opposite lateral root phenotype with the double mutant of CEP receptors, cepr1 cepr2, suggests that RLK68 and RLK165 play negative roles in the CEP-CEPR-mediated signaling pathway. In this proposal we would like to investigate the possible interrelationships between RLK68/RLK165 and PIN1, and between RLK68/RLK165 and the CEP-CEPR signaling pathway. We plan to elucidate the RLK68/RLK165-mediated signaling pathway from ligand perception to downstream target genes. Furthermore, based on the expression patterns of all LRR-RLKs, we propose to identify additional LRR-RLKs which are involved in lateral root development.