THESIS
2007
xvii, 136 leaves : ill. (some col.) ; 30 cm
Abstract
The development of sensory organ requires a coordinated expression of transcription factors and their downstream targets. Although the nature of these genes and their regulatory mechanisms are not well defined, they facilitate the organ assembly process. Using the male sensory ray in Caenorhabditis elegans as a model and a missing ray mutant KC62, a novel bona fide organ assembly process was defined where differentiated ray cells organize themselves as a functional organ. The assembly defect in KC62 is caused by high copy number of a transgenic fragment of ram-5 promoter. By deletion analysis on this fragment, a 123 bp region was identified to be responsible for the missing ray phenotype and ram-5 reporter expression in ray structural cells. Two putative binding sites of the homeobox t...[
Read more ]
The development of sensory organ requires a coordinated expression of transcription factors and their downstream targets. Although the nature of these genes and their regulatory mechanisms are not well defined, they facilitate the organ assembly process. Using the male sensory ray in Caenorhabditis elegans as a model and a missing ray mutant KC62, a novel bona fide organ assembly process was defined where differentiated ray cells organize themselves as a functional organ. The assembly defect in KC62 is caused by high copy number of a transgenic fragment of ram-5 promoter. By deletion analysis on this fragment, a 123 bp region was identified to be responsible for the missing ray phenotype and ram-5 reporter expression in ray structural cells. Two putative binding sites of the homeobox transcription factor distal-less/Dlx were identified in this region accounting for these phenomena. Animals display ray assembly and attachment defects when the activity of the distal-less homolog in C. elegans, ceh-43, is attenuated. Reduction of the ram-5 reporter signal was also observed. The temporal and spatial expression of ceh-43 revealed by gfp reporters was detected in structural cells throughout the whole ray assembly process. By the same reporter, expression of ceh-43 was determined to be dependent of lin-32 activity. ceh-43 was also shown to control the expression of mab-22 transcriptional reporter. To decipher what target genes ceh-43 regulates and how they governs the ray assembly process, phylogenetic footprinting was used to perform a genome-wide evaluation of the downstream targets. The data set so obtained was further integrated with the C. elegans male tail RNAi phenome data set. 41 predicted ceh-43 targets were identified with ray missing, fusion or Ram phenotype upon RNAi knock down. The characterization of these gene and their functional roles in the ray assembly will allow us to establish a mechanistic understanding of organ formation, which can be evaluated in the future by molecular and genetic means.
Post a Comment