Stenvik Grethe-Elisabeth, Tandstad Nora M, Guo Yongfeng, Shi Chun-Lin, Kristiansen Wenche, Holmgren Asbjørn, Clark Steven E, Aalen Reidunn B, Butenko Melinka A
Department of Molecular Biosciences, University of Oslo, N-0316 Oslo, Norway.
Plant Cell. 2008 Jul;20(7):1805-17. doi: 10.1105/tpc.108.059139. Epub 2008 Jul 25.
In Arabidopsis thaliana, the final step of floral organ abscission is regulated by INFLORESCENCE DEFICIENT IN ABSCISSION (IDA): ida mutants fail to abscise floral organs, and plants overexpressing IDA display earlier abscission. We show that five IDA-LIKE (IDL) genes are expressed in different tissues, but plants overexpressing these genes have phenotypes similar to IDA-overexpressing plants, suggesting functional redundancy. IDA/IDL proteins have N-terminal signal peptides and a C-terminal conserved motif (extended PIP [EPIP]) at the C terminus (EPIP-C). IDA can, similar to CLAVATA3, be processed by an activity from cauliflower meristems. The EPIP-C of IDA and IDL1 replaced IDA function in vivo, when the signal peptide was present. In addition, synthetic IDA and IDL1 EPIP peptides rescued ida and induced early floral abscission in wild-type flowers. The EPIP-C of the other IDL proteins could partially substitute for IDA function. Similarly to ida, a double mutant between the receptor-like kinases (RLKs) HAESA (HAE) and HAESA-LIKE2 (HSL2) displays nonabscising flowers. Neither overexpression of IDA nor synthetic EPIP or EPIP-C peptides could rescue the hae hsl2 abscission deficiency. We propose that IDA and the IDL proteins constitute a family of putative ligands that act through RLKs to regulate different events during plant development.
在拟南芥中,花器官脱落的最后一步受脱落缺陷花序(IDA)调控:ida突变体无法使花器官脱落,而过表达IDA的植株则表现出提前脱落。我们发现五个类IDA(IDL)基因在不同组织中表达,但过表达这些基因的植株具有与过表达IDA的植株相似的表型,这表明它们存在功能冗余。IDA/IDL蛋白具有N端信号肽和C端保守基序(扩展PIP [EPIP])位于C末端(EPIP-C)。与CLAVATA3类似,IDA可被来自花椰菜花分生组织的一种活性物质加工处理。当信号肽存在时,IDA和IDL1的EPIP-C在体内取代了IDA的功能。此外,合成的IDA和IDL1的EPIP肽挽救了ida突变体,并在野生型花朵中诱导了早期花器官脱落。其他IDL蛋白的EPIP-C可部分替代IDA的功能。与ida类似,类受体激酶(RLK)HAESA(HAE)和类HAESA2(HSL2)之间的双突变体表现出花不脱落的现象。过表达IDA或合成的EPIP或EPIP-C肽均无法挽救hae hsl2的脱落缺陷。我们提出,IDA和IDL蛋白构成了一个假定的配体家族,它们通过RLK发挥作用,以调控植物发育过程中的不同事件。