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Dissecting the molecular basis and assembly of a complex morphological trait

剖析复杂形态特征的分子基础和组装

基本信息

批准号：
8861499
负责人：
Peter Andolfatto
金额：
$ 45.78万
依托单位：
PRINCETON UNIVERSITY
依托单位国家：
美国
项目类别：
财政年份：
2015
资助国家：
美国
起止时间：
2015-05-01 至 2019-01-31
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/8861499
关键词：
Abdomen Address Affect Alleles Behavior Biological Models Biology Chromosomes Chromosomes, Human, Pair 3 Clustered Regularly Interspaced Short Palindromic Repeats Color Complex Control Locus DNA Development Dissection Drosophila genus Drosophila melanogaster Enzymes Event Evolution Exhibits Gene Mutation Genes Genetic Techniques Genome Genomics Goals Human In Situ Hybridization Individual Island Knowledge Lead Life Literature Maps Modeling Molecular Molecular Genetics Molecular Profiling Morphology Mutation Pathway interactions Pattern Phenotype Pigmentation physiologic function Pigments Polygenic Traits Population Process Proteins Quantitative Trait Loci Regulation Relative (related person)Research Resistance Role Rosa Shapes System Techniques Time Transgenic Organisms Uncertainty Variant Work base functional genomics gene function genetic evolution genome editing genome-wide male mutant population survey public health relevance reconstruction sample fixation trait transcriptome sequencing

项目摘要

DESCRIPTION (provided by applicant): The goal of this research is to dissect the causative genes and mutations underlying a complex trait, and trace the stepwise process by which the identified causative alleles arose and spread through an isolated population to generate a fixed morphological phenotype. The species Drosophila santomea exhibits a recently evolved, drastic shift in its pigment patterns that represents an optimal model system in which to dissect complex polygenic traits. Our previous work identified the gene underlying one of four major QTL contributing to this trait. Analysis of multiple individuals in the population revealed that causative alleles of this gene arose several times in parallel in the D. santomea population (i.e. a "soft sweep"). Here, we propose to employ molecular genetic techniques (introgression mapping and transgenic complementation) to identify causative genes and mutations responsible for two additional QTL. Using a combination of molecular and genomic techniques (in situ hybridization, RNA-seq), we will then assess how these loci interact with each other, as well as how they impact the genome-wide profile of expression. Finally, we will survey population variation at these additional causative loci to assess whether a similar soft sweep occurred, and determine whether these genes exhibit signs of positive selection. This study will provide a rare vista of a complex morphological trait that integrates molecular studies of gene function with processes occurring at the population level.