The <i>Ligon lintless</i><i>-2</i> Short Fiber Mutation Is Located within a Terminal Deletion of Chromosome 18 in Cotton
Jinesh D. Patel, Xianzhong Huang, Lifeng Lin, Sayan Das, Rahul Chandnani, Sameer Khanal, Jeevan Adhikari, Tariq Shehzad, Hui Guo, Eileen M. Roy-Zokan, Junkang Rong, Andrew H. Paterson
Abstract
Extreme elongation distinguishes about one-fourth of cotton (Gossypium sp.) seed epidermal cells as "lint" fibers, useful for the textile industry, from "fuzz" fibers (,5 mm). Ligon lintless-2 (Li 2 ), a dominant mutation that results in no lint fiber but normal fuzz fiber, offers insight into pathways and mechanisms that differentiate spinnable cotton from its progenitors. A genetic map developed using 1,545 F2 plants showed that marker CISP15 was 0.4 cM from Li 2 , and "dominant" simple sequence repeat (SSR) markers (i.e. with null alleles in the Li 2 genotype) SSR7 and SSR18 showed complete linkage with Li 2 . Nonrandom distribution of markers with null alleles suggests that the Li 2 phenotype results from a 176-to 221-kb deletion of the terminal region of chromosome 18 that may have been masked in prior pooled-sample mapping strategies. The deletion includes 10 genes with putative roles in fiber development. Two Glycosyltransferase Family 1 genes showed striking expression differences during elongation of wild-type versus Li 2 fiber, and virus-induced silencing of these genes in the wild type induced Li 2 -like phenotypes. Further, at least 7 of the 10 putative fiber development genes in the deletion region showed higher expression in the wild type than in Li 2 mutants during fiber development stages, suggesting coordinated regulation of processes in cell wall development and cell elongation, consistent with the hypothesis that some fiber-related quantitative trait loci comprise closely spaced groups of functionally diverse but coordinately regulated genes.