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Extreme elongation distinguishes about one-fourth of cotton ( Gossypium sp.) seed epidermal cells as "lint" fibers, useful for the textile industry, from "fuzz" fibers (&lt;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.

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