| Lab overview: There are several active lines of investigation in my lab that are mutually independent and thematically converge on understanding the role of stress response signaling in disease and development. Projects in the lab are directed at uncovering new mechanisms of mRNA translation regulation during cellular stress (e.g. PMID32938929), the phenotypic consequences of disrupting stress response signaling in metabolic tissues (e.g. PMID 38457339), and the role of these signaling pathways in visual system development and disease (e.g. PMID 34919148). The lab uses a potent combination of Drosophila (fruit fly) model, cultured human cells, and classic biochemistry approaches to comprehensively map the molecular mechanisms and physiological relevance of stress response signaling. |
Rotation/thesis project: We recently discovered that loss of the stress response transcription factor, ATF4, results in cell migration defects using the Drosophila ovary as a model (see figure showing live imaging of migrating ‘border’ cells in green making their way through germline cells in red). Though ATF4 is a well-studied transcription factor, its role in collective cell migration is unknown. This is worth investigating particularly because ATF4 and associated stress response pathway components are frequently upregulated in many cancers. Open questions include:
1) How are ATF4 levels regulated in migrating cells?
2) What are the binding partners of ATF4 in migrating cells?
3) What are the transcriptional targets of ATF4 that effect migration?
The project(s) will use a potent combination of Drosophila genetics, live imaging, and cell culture experiments to examine the above questions.