Genetic Analysis, Gene Fine-Mapping And Expression Profile Of Short Fiber Mutants In Upland Cotton

Upland cotton is the world’s leading cotton cultivars. The cotton fiber developed from the epidermis of ovules outer integument, is one of the most important textile materials and has important economic value in the world. Up to now, two kinds of short fiber mutations were found in the fiber elongation and they were named Li1 and Li2, respectively. Because of dominant lethal effect in homozygous plants, we can only obtain heterozygous Li1 mutant and wild type plants. Illuminating the forming mechanisms of short fiber will not only enable us to better understand the mechanism of cotton fiber elongation, but also help us improve cotton yield and fiber quality through molecular design. In this paper, we have studied the genetic and molecular mechanism of fiber elongation by using two types of short fiber mutations, Li1 and Li2. The main results are as follows:In this study, we firstly developed two backcross populations:(Li1×Hai7124) (Ligon lintless)xHai7124 and li1×(Li×Hai7124) (Ligon lintless) to construct a high-resolution genetic map of Li1 gene. In the first BC1 population, Li1 gene was mapped between G39 and G50, and they had a genetic distance of 0.595cM and 0.445cM from Li1 gene, respectively. In the second BC1 population, Li1 was mapped between G57 and G49, and they had a genetic distance of 0.185cM and 0.239cM from Lij gene, respectively. An integrated genetic map was constructed from two different BC1 populations according to their mutual parent Li1 and SSR markers. Li1 gene was mapped between G49 and G50 in this integrated genetic map, and they had a genetic distance of 0.173cM and 0.180cM from Li1 respectively. This result laid a solid foundation for map-based cloning of the Li1 gene.We also developed two F2 populations:(Li2xHai7124)F2 and (Li2×ssubl8)F2 for fine mapping the Li2 gene. In the first F2 population, Li2 gene was located on the end of chr. 18, and the nearest marker Z08 had a genetic distance of 6.05 1cM from Li2. In the second F2 population, Li2 was also located on the end of chr.18, but the nearest marker Z08 was 9.266cM from Li2.To conduct competitive chips hybridization, mutant Li1 was paired with li1, and Li2 paired with sub 18, respectively. These two competitive chips we referred to Li1-chip and Li2-chip, respectively. There are 589 and 437 differentially expressed genes in the Li1-and Li2-chip, respectively. Among them, only 6 ESTs identical in differential expressed ESTs between Li1-and Li2-chip. The rest of the differentially expressed ESTs between Li1-and Li2-chip, are not synchronized in differential expression. Differentially expressed genes in Li1 and Li2-chip, are classified in the molecular function, biological process, or in the cellular component. However, every kinds of differentially expressed genes in Lii-and Li2-chip are quite different, indicated different molecular mechanism of the formation of short fibers in mutants Li1 and Li2. In addition, there were 13 differential expressed ESTs related to the oxidase or peroxidase and 26 differential expressed ESTs related to the transcriptional factors in Li1-chip. And these differentially expressed genes may be related to the formation of short fiber of mutant Li1.With the F2 and BC1 populations developed from Li1 mutant, we verified the lethal effect on homozygous dominant mutant Li1. During studying the interaction between genes controlled Li1 and fiber less phenotype, we firstly identified a new Li1 mutant, which do not have lethal effect on this homozygous mutant. Three F2 segregating populations Li-R×TM-1, Li-R×Hai7124 and Li-R×Li1 were developed to study the inheritance of recombinant mutant Li-R. The results showed that the homozygous-dominant-survive phenotype controlled by two genes:dominant Li1 gene and recessive lia. The gene lia derived from XZ142 FLM was firstly found in this study. Therefore, the genotype for the homozygous-dominant-survive phenotype of Li-R was liaLiiLii, while the genotype for the homozygous-dominant-lethal phenotype of Li1 mutant was LiaLiaLi1Li1. An (Li-R×TM-1)F2:3 was used to analyze allelism of our new gene lia, and the results showed that lia was not in the same gene allele with genes li3 and n2, which were related to the fiber initiation.