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JXB Advance Access published online on March 5, 2007

Journal of Experimental Botany, doi:10.1093/jxb/erl243
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© The Author [2007]. Published by Oxford University Press [on behalf of the Society for Experimental Biology]. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org

RESEARCH PAPER

Genetic control of pungency in C. chinense via the Pun1 locus

Charles Stewart, Jr1, Michael Mazourek1, Giulia M. Stellari1, Mary O'Connell2 and Molly Jahn1,*

1Department of Plant Biology, Cornell University, Ithaca, NY 14853, USA
2Department of Plant and Environmental Sciences, New Mexico State University, Las Cruces, NM 88003, USA

* Present address and to whom correspondence should be sent: CALS Dean's Office, 140 Agriculture Hall, 1450 Linden Dr., University of Wisconsin–Madison, Madison, WI 53706, USA. E-mail: mmj9{at}cornell.edu

Capsaicin, the pungent principle in hot peppers, acts to deter mammals from consuming pungent pepper pods. Capsaicinoid biosynthesis is restricted to the genus Capsicum and results from the acylation of the aromatic compound, vanillylamine, with a branched-chain fatty acid. The presence of capsaicinoids is controlled by the Pun1 locus, which encodes a putative acyltransferase. In its homozygous recessive state, pun1/pun1, capsaicinoids are not produced by the pepper plant. HPLC analysis confirmed that capsaicinoids are only found in the interlocular septa of pungent pepper fruits. Immunolocalization studies showed that capsaicinoid biosynthesis is uniformly distributed across the epidermal cells of the interlocular septum. Capsaicinoids are secreted from glandular epidermal cells into subcuticular cavities that swell to form blisters along the epidermis. Blister development is positively associated with capsaicinoid accumulation and blisters are not present in non-pungent fruit. A genetic study was used to determine if the absence of blisters in non-pungent fruit acts independently of Pun1 to control pungency. Screening of non-pungent germplasm and genetic complementation tests identified a previously unknown recessive allele of Pun1, named pun12. Sequence analysis of pun12 revealed that a four base pair deletion results in a frameshift mutation and the predicted production of a truncated protein. Genetic analysis revealed that pun12 co-segregated exactly with the absence of blisters, non-pungency, and a reduced transcript accumulation of several genes involved in capsaicinoid biosynthesis. Collectively, these results establish that blister formation requires the Pun1 allele and that pun12 is a recessive allele from C. chinense that results in non-pungency.

Key words: Blister, capsaicin, capsaicinoids, Capsicum, pepper, pungency, secretion

Received 27 June 2006; Revised 3 October 2006 Accepted 9 October 2007


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