Neodiversification of homeologous CLAVATA1-like receptor kinase genes in soybean leads to distinct developmental outcomes
Abstract The CLAVATA pathway that regulates stem cell numbers of the shoot apical meristem has exclusively been studied in Arabidopsis; as such insight into other species is warranted. In this study, a GmCLV1A mutant (F-S562L) with altered lateral organ development, and two mutants of GmNARK, isolat...
Guardado en:
| Autores principales: | , , , , , , |
|---|---|
| Formato: | article |
| Lenguaje: | EN |
| Publicado: |
Nature Portfolio
2017
|
| Materias: | |
| Acceso en línea: | https://doaj.org/article/9c76137ecbc94d8797032730aea18ee5 |
| Etiquetas: |
Agregar Etiqueta
Sin Etiquetas, Sea el primero en etiquetar este registro!
|
| Sumario: | Abstract The CLAVATA pathway that regulates stem cell numbers of the shoot apical meristem has exclusively been studied in Arabidopsis; as such insight into other species is warranted. In this study, a GmCLV1A mutant (F-S562L) with altered lateral organ development, and two mutants of GmNARK, isolated from a Forrest M2 population (EMS-mutated soybean) were studied. GmCLV1A and GmNARK encode for LRR receptor kinases, and share 92% of protein sequence. While GmNARK is critical for systemic regulation of nodulation (new organ made on the root through symbiosis), we show that GmCLV1A functions locally and has no apparent function in nodulation or root development. However, a recessive, loss-of-function mutation (S562L) in a putative S-glycosylation site of GmCLV1A causes stem nodal identity alterations as well as flower and pod abnormalities (deformed flower and pod). The mutant also exhibits a homeotic phenotype, displaying abnormal leaf development/number, vein-derived leaf emergence, and a thick, faciated stem. The mutant phenotype is also temperature-sensitive. Interestingly, a novel truncated version of GmCLV1A was identified upstream of GmCLV1A that is absent from GmNARK, but is present upstream of the GmNARK orthologues, MtSUNN and PvNARK. Taken together, our findings indicate that GmCLV1A acts on shoot architecture, whereas GmNARK, functions in controlling nodule numbers. |
|---|