Danielle Herrig and Changya Chen will present their research on June 6, 2013
Danielle’s Research Abstract:
THE MOLECULAR BASIS OF THE LARGE X-EFFECT IN DROSOPHILA: GENE EXPRESSION ANALYSES IN HYBRIDS
One of the main rules of speciation is the Large X-effect, which posits that the X chromosome has a disproportionate influence on hybrid male sterility compared to autosomes, which may be explained by faster-X evolution.Microarray analyses in our lab utilizing Drosophila yakuba and D. santomea show that genes on the X chromosome are more prone to be differentially expressed between these species than autosomal genes, and that this rapid X-linked evolution is driven by Darwinian selection. Interestingly, hybrid misexpression (expression that is not the same or the intermediate of the parental species) occurs more frequently on autosomes than on the X chromosome. The observation that X-linked genes are more differentially expressed in the species but autosomal genes are preferentially misexpressed in hybrids initially seems contradictory. One possible explanation of this apparent contradiction is that X-linked trans-regulatory factors influence the expression of genes on autosomes by co-evolving cis-regulatory elements. I hypothesize that both the rapid evolution of X-linked trans-regulatory elements and their hemizygosity in males contribute to widespread autosomal misexpression in hybrids as a result of the preferential recognition of cis-regulatory elements by conspecific trans-regulatory elements. This hypothesis will be tested by 1) determining the effects of X chromosome hemizygosity on autosomal misexpression in hybrids and 2) identifying trans-regulatory elements located on the X chromosome associated with autosomal misexpression in hybrid males.
Changya’s Research Abstract:
Epigenetic and transcriptional regulation for maturation of murine hematopoietic stem cells
Hematopoiesis is a crucial developmental process in mammals. In this process, hematopoietic stem cells (HSC) are capable of self-renewal and differentiation into all blood cell types. During adult, HSCs reside in the bone marrow in a quiescent state. In the embryonic stage, the development of HSCs is sequentially found in several niches. Definitive adult-type HSCs are born in the E10.5 aorta-gonads-mesonephros (AGM), and thereafter are colonized to the fetal liver (FL), placenta, and bone marrow. The emergence of HSC is still controversial issue. Recent studies have illustrated that HSCs emerge from a subset of endothelial cells in the AGM region. In the past decade, adult HSCs have been extensively studied using global epigenomic profiling and transcriptional profiling, which provided novel insight into their functions and clinic features. However, it is still a challenge to discover the epigenomic and transcriptional landscape during the embryonic development of HSCs. We plan to perform ChIP-Seq technology using limited number of in vivo cells, which are gathering from three different mouse HSC developmental niches, E11.5 AGM, E14.5 FL, and adult bone marrow. Five histone modifications, including H3K4Me1, H3K4Me3, H3K9Me3, H3K27Me3, and H3K27Ac, will be detected globally in three development stages. According to the histone modification profiling, we will identify novel stage-specific enhancers, which regulate HSCs maturation. Further, key transcription factor that control the HSCs development will be concerned. Runx1 is an important transcription factor in the emergence of HSC. We plan to discover its global regulation pattern in the process of HSC maturation. Overall, the on-going project will provide a comprehensive epigenomic and transcriptional profiling for the early HSCs emergence and development.