Ectopic expression of the Coffea canephora SERK1 homolog‐induced differential transcription of genes involved in auxin metabolism and in the developmental control of embryogenesis
2018
Pérez‐Pascual, Daniel | Jiménez‐Guillen, Doribet | Villanueva‐Alonzo, Hernán | Souza‐Perera, Ramón | Godoy‐Hernández, Gregorio | Zúñiga‐Aguilar, José Juan
Somatic embryogenesis receptor‐like kinase 1 (SERK1) is a membrane receptor that might serve as common co‐regulator of plant cell differentiation processes by forming heterodimers with specific receptor‐like kinases. The Coffea canephora SERK1 homolog (CcSERK1) was cloned in this work, and its early function in the transcription of embryogenesis master genes and of genes encoding proteins involved in auxin metabolism was investigated by externally manipulating its expression in embryogenic leaf explants, before the appearance of embryogenic structures. Overexpression of CcSERK1 early during embryogenesis caused an increase in the number of somatic embryos when the 55‐day process was completed. Suppression of CcSERK1 expression by RNA interference almost abolished somatic embryogenesis. Real time‐PCR experiments revealed that the transcription of the CcAGL15, CcWUS, CcBBM, CcPKL, CcYUC1, CcPIN1 and CcPIN4 homologs was modified in direct proportion to the expression of CcSERK1 and that only CcLEC1 was inversely affected by the expression levels of CcSERK1. The expression of the CcYUC4 homolog was induced to more than 80‐fold under CcSERK1 overexpression conditions, but it was also induced when CcSERK1 expression was silenced. The level of CcTIR1 was not affected by CcSERK1 overexpression but was almost abolished during CcSERK1 silencing. These results suggest that CcSERK1 co‐regulates the induction of somatic embryogenesis in Coffea canephora by early activation of YUC‐dependent auxin biosynthesis, auxin transport mediated by PIN1 and PIN4, and probably auxin perception by the TIR1 receptor, leading to the induction of early‐stage homeotic genes (CcAGL15, CcWUS, CcPKL and CcBBM) and repression of late‐stage homeotic genes (CcLec1).
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