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Multiple Non-pungent Capsicum chinense Accessions with a Loss of Function CaKR1 Allele Originating from South America
Horticulture Journal ( IF 1.2 ) Pub Date : 2020-07-21 , DOI: 10.2503/hortj.utd-184
Sota Koeda 1 , Ryutaro Nakano 1 , Takaya Sawaki 2 , Kosuke Sato 2 , Yoshiyuki Tanaka 2 , Shinya Kanzaki 1
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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.



中文翻译:

来自南美的多个丧失功能的CaKR1等位基因的非辛辣辣椒种质

辣椒中据报道酰基转移酶Pun1),推定的氨基转移酶pAMT),推定的酮酰基-ACP还原酶CaKR1)和R2R3-MYB转录因子CaMYB31)的功能缺失是导致非刺激性的遗传原因。在本研究中,245 C. chinense最初对种质进行了非辛辣特性的筛选。通过品尝试验选择了识别号分别为3327、3356、3529、4026、4028和4034的六种候选物,并通过高效液相色谱法确定了非辛辣性分析。表达和序列分析推断3529号的非刺激性是由于Pun1的非表达。对pAMT的分析证实了3356号(专利5)和4034号(专利9)具有功能缺失突变。因为3327号,4026号和4028号的非刺激性似乎不是由Pun1pAMT的突变引起的,所以CaKR1使用基于聚合酶链反应的共显性标记进一步检查突变。基因分型明确了3327号,4026号和4028号与非刺激性3341号具有相同的CaKR1等位基因突变。此外,与刺激性哈瓦那人和3341号的交叉测试清楚地表明,No.3327No.4026No.4028CaKR1功能缺失的结果。我们以前和现在的研究已经表明,非刺激性品种C.楸拥有的pAMT广泛分布于中美洲,南美洲和西印度群岛(加勒比海),非刺激性品种具有Cakr1来自玻利维亚和秘鲁。基于本地产地对非辛辣辣椒的偏爱,可能已经进行了一些人工选择。

更新日期:2020-08-23
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