The <i>Ligon lintless</i><i>-2</i> Short Fiber Mutation Is Located within a Terminal Deletion of Chromosome 18 in Cotton

Abstract

Extreme elongation distinguishes about one-fourth of cotton (<i>Gossypium</i> sp.) seed epidermal cells as "lint" fibers, useful for the textile industry, from "fuzz" fibers (<5 mm). <i>Ligon lintless-2</i> (<i>Li</i> _<i>2</i> ), 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 <i>Li</i> _<i>2</i> , and "dominant" simple sequence repeat (SSR) markers (i.e. with null alleles in the <i>Li</i> _<i>2</i> genotype) SSR7 and SSR18 showed complete linkage with <i>Li</i> _<i>2</i> Nonrandom distribution of markers with null alleles suggests that the <i>Li</i> _<i>2</i> 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 <i>Li</i> _<i>2</i> fiber, and virus-induced silencing of these genes in the wild type induced <i>Li</i> _<i>2</i> <i>-</i>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 <i>Li</i> _<i>2</i> 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.