Multiple non-pungent capsicum Chinense accessions with a loss of function CaKR1 allele originating from South America

Abstract

In Capsicum, loss of function mutation of acyltransferase (Pun1), putative aminotransferase (pAMT), putative ketoacyl-ACP reductase (CaKR1), and R2R3-MYB transcription factor (CaMYB31) have been reported to be the genetic causes of non-pungency. In the present study, 245 C. chinense accessions were initially screened for non-pungency attributes. Six candidates with identification numbers, No. 3327, No. 3356, No. 3529, No. 4026, No. 4028, and No. 4034 were selected by tasting test, and the non-pungency attribute was confirmed by high-performance liquid chromatographic analysis. Expression and sequence analysis inferred that the non-pungency of No. 3529 was due to the non-expression of Pun1. Analysis of pAMT confirmed that No. 3356 (pamt5) and No. 4034 (pamt9) had loss of function mutations. Because the non-pungency of No. 3327, No. 4026, and No. 4028 did not seem to be caused by mutation of either Pun1 or pAMT, the CaKR1 mutation was further examined using a polymerase chain reaction-based, co-dominant marker. Genotyping clarified that No. 3327, No. 4026, and No. 4028 had the same mutated CaKR1 allele as non-pungent No. 3341. Moreover, a crossing test with a pungent Habanero and No. 3341 clearly revealed that the non-pungency in No. 3327, No. 4026, and No. 4028 was a result of a loss of function mutation of CaKR1. Our previous and present studies have shown that non-pungent cultivars of C. chinense possessing pamt are widely distributed in Central America, South America and the West Indies (Caribbean), while non-pungent cultivars possessing Cakr1 originate from Bolivia and Peru. Some artificial selection may have occurred that was based on a preference for non-pungent peppers in the local region of origin.