Project Summaries

12-210  Project Manager: D. C. Jones


Marina Naoumkina, USDA-ARS

The cotton (Gossypium hirsutum L.) fiber mutation, Ligon lintless-2, is controlled by a single dominant gene (Li2) and results in extremely shortened lint fibers on mature seeds with no visible pleiotropic effects on vegetative growth and development. The Li2 mutant phenotype provides an ideal model system to study fiber elongation. To understand metabolic processes involved in cotton fiber elongation, changes in metabolites and transcripts in the Li2 mutant fibers were compared to wild-type fibers during development. A significant reduction of all detected free sugars, sugar alcohols, sugar acids, and sugar phosphates were observed in mutant fibers. Biological processes associated with carbohydrate biosynthesis, cell wall loosening, and cytoskeleton were down-regulated in Li2 fibers.  Gamma-aminobutyric acid, known as a signaling factor in many organisms, was significantly elevated in mutant fibers. Higher accumulation of 2-ketoglutarate, succinate, and malate suggested higher nitrate assimilation in the Li2 line. Levels of nitrogen transport amino acids along with transcriptional activation of genes involved in nitrogen compound metabolism, including biosynthesis glutamine family amino acids and nucleic acids, suggest re-direction of carbon flow into nitrogen metabolism in Li2 mutant fibers. This report provides the first comprehensive analysis of metabolite and transcript changes in response to Li2 mutation in elongating fibers. A number of factors associated with cell elongation found in this study will facilitate further research in understanding metabolic processes of cotton fiber elongation.

Discovery of the Li2 gene would greatly expand our knowledge of the molecular mechanisms and regulatory elements controlling fiber elongation. Understanding these developmental and regulatory events can provide a means by which fiber length can be manipulated and potentially improved. Therefore during 2012 year we made a lot of efforts to narrow dawn the Li2 locus. Linkage mapping was conducted in a F2 population consisting of 536 individuals developed from a cross between homozygous dominant mutant Li2Li2 and homozygous recessive WT Li2Li2 parents. Using SSR and newly developed SNP markers we were able to narrow down the mutation locus up to a 2.7 cM region that corresponds to 574 kb of genomic region (consisting 90 putative genes) on chromosome 13 of G. raimondii reference genome. Our future work will focus on creating a larger F2 population and developing new SNP markers to locate the mutant gene.


Project Year: 2012

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