Understanding the Cotton Fiber Elongation Process Using Short Fiber Mutants, the Ligon Lintless-1 (Li1) and -2 (Li2) as an Experiment Model System

The length of cotton fiber is an important agronomic trait that directly affects the quality of yarn. Understanding the molecular basis of fiber elongation would provide a means for improvement of fiber length. Ligon lintless-1 (Li1) and Ligon lintless-2 (Li2) are monogenic and dominant mutations that result in an extreme reduction in the length of lint fiber. A defect in the Li1 locus affected a number of traits (dwarf deformed plants and short fiber phenotype), while the defect in Li2 locus affected only fiber length. Therefore, the Li1 and Li2, most likely, are different types of genes; their alterations interrupt different parts of a complex biosynthetic process, but in both cases cause a short fiber phenotype. In this regard these two mutants are a useful model system to study cotton fiber elongation. We have recently mapped the Li1 and Li2 loci within 2.7 and 0.3 centimorgans, respectively. Analysis of expression level of genes in the Li2 locus suggested 2 putative candidates. Functions of these genes are under investigation in cotton. We have investigated global transcript and metabolite changes in developing fiber cells of the Li1 and Li2. We found that the aquaporins were the most down-regulated gene family in both short fiber mutants. The osmolality and concentrations of soluble sugars were less in saps of the Li1 and Li2, whereas the concentrations of malic acid, potassium and other detected ions were significantly higher in saps of mutants than in WT. These results suggest that higher accumulation of ions in fiber cells of the Li1 and Li2 may be the result of limited uptake of water due to a combination of factors, such as reduced osmotic pressure and low expression of aquaporins, causing cessation of fiber elongation. I will present our recent progress toward a better understanding of cotton fiber elongation.