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High-probability grants
According to our matching algorithm, Matthew Slattery is the likely recipient of the following grants.
Years |
Recipients |
Code |
Title / Keywords |
Matching score |
2009 — 2011 |
Slattery, Matthew |
F32Activity Code Description: To provide postdoctoral research training to individuals to broaden their scientific background and extend their potential for research in specified health-related areas. |
Indentification of Hox Target Genes Controlling Tissue Growth @ Columbia University Health Sciences
DESCRIPTION (provided by applicant): Disruption of tissue growth and patterning is a common step in the development of cancer, and proper tissue morphology depends upon combined input from intercellular signaling pathways and region-specific transcription factors. In Drosophila melanogaster the protein Ultrabithorax (Ubx), a region-specific transcription factor and member of Hox family of homeodomain proteins, restricts growth of hindwing (haltere) tissue in part by modulating the expression of several components of the mitogenic Decapentaplegic (Dpp) pathway. The goal of this project is to identify target genes and transcriptional regulatory elements in the Drosophila genome that are directly regulated by Ubx in the haltere;three experimental approaches will be used to accomplish this goal. First, a novel gene expression profiling .method will be used to analyze regional gene expression differences in serially homologous Ubx-expressing (haltere) and non-expressing (wing) tissues. The second step will use chromatin immunoprecipitation and DamID in combination with Drosophila genome tiling arrays to determine the DNA regions that are directly bound by Ubx in the haltere. Together, these experiments will allow the identification of direct Ubx target genes in the haltere on a genome-wide scale. The third step in this analysis will be to use Cognate Site Identity (CSI) microarray technology to characterize the DNA-binding specificity of Ubx, both as a monomer and in conjunction with the Hox cofactors Extradenticle (Exd) and Homothorax (Hth). This will permit exploration of the DNA sequences to which Ubx can and cannot bind, and, in combination with the first two steps, should allow a better understanding of a Hox regulatory network. Follow-up analysis on a subset of Ubx target genes, particularly those likely to be involved in growth regulation, will include the validation of their expression patterns in both the wing and haltere and functional analysis using standard Drosophila genetic approaches. Public Health Relevance: The Hox proteins and many of the signaling molecules controlling growth, proliferation and morphogenesis are conserved between Drosophila and humans;the goal of this research is to provide insight into the mechanisms by which a Hox transcription factor regulates tissue growth. Ultimately, a detailed description of how Hox proteins regulate tissue growth during normal development will be crucial to understanding their role when growth is misregulated in diseases states such as cancer.
|
0.964 |
2016 — 2020 |
Slattery, Matthew |
R35Activity Code Description: To provide long term support to an experienced investigator with an outstanding record of research productivity. This support is intended to encourage investigators to embark on long-term projects of unusual potential. |
Regulatory Precision in Stress Responsive Transcriptional Networks @ University of Minnesota
PROJECT SUMMARY Many cellular challenges ? chemical, metabolic, and physical ? generate reactive oxygen species (ROS), which have the potential to damage macromolecules including proteins, lipids, and nucleic acids. Members of the Cap-n-Collar (CNC) transcription factor family, including NRF2, regulate antioxidant gene expression and mitigate ROS-mediated damage. These opposing oxidant and antioxidant forces must be precisely balanced: too little NRF2 and excess ROS cause cell damage and mutation, whereas too much NRF2 gives cells a dangerous proliferative advantage. To fully understand the mechanistic implications of NRF2 activation we need a comprehensive view of its regulatory network, yet surprisingly little is known about the global reach of NRF2's regulatory activity and how it integrates with additional stress-responsive transcription factors. We will use a combination of hypothesis-driven genomics and focused biological validation experiments to provide both systems level and mechanistic insights into the NRF2 regulatory network and consequences of its activation. Importantly, this work will also address issues regarding the general principles of transcriptional regulatory precision, including: (1) how transcription factor DNA binding properties and combinatorial transcription factor interactions integrate to drive graded versus switch-like gene expression, (2) the dynamics and cell-type specificity of rapid transcriptional reprogramming in human cells, (3) how variation in cis- regulatory DNA is functionally linked to disease risk, and (4) the mechanisms of cell autonomous and non- autonomous regulatory network propagation. These are relevant issues for all transcriptional regulators, so the knowledge gained in the context of NRF2-mediated gene regulation will also extend to additional transcription factor families.
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