Abstract
Papaya (Carica papaya L.) is an important tropical fruit crop globally, although it is hampered by papaya ringspot virus type P (PRSV-P). Previous genetic research discovered a functional PRSV-P resistance marker in a mapping population of F2 plants of Vasconcellea pubescens (resistant to PRSV-P) × Vasconcellea parviflora (susceptible to PRSV-P) and showed that the marker exhibited homology to a serine threonine protein kinase (STK) gene. In this study, the susceptibility of Carica and Vasconcellea towards Papaya Ringspot Virus type P (PRSV-P) was analysed through structural differences of STK gene. Full length cDNAs of putative PRSV-P resistance genes designated CP STK from C. papaya and VP STK1 and VP STK2 from V. pubescens were cloned by rapid amplification of cDNA ends (RACE). Because of a frame-shift mutation, the two homologous sequences are transcribed and processed differentially in V. pubescens, resulting in two distinct transcripts in V. pubescens, but they are fused into a single message in C. papaya. The functional source of PRSV resistance in V. pubescens could be a peroxisomal targeting signal (PTS2) found in VP STK2 but not in the other transcripts. The STK gene in V. pubescens may have been derived by resistance-inducing alternative splicing. VP STK2, a putative resistance gene discovered in this work, could be a novel source of PRSV-P resistance for papaya genotypes.
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