How do individual cells in an embryo know who they are and where to go?
In the Rogers Lab, we explore the molecular logic that guides cell fate decisions, morphogenesis, and migration during early vertebrate development. Our work focuses on uncovering how cells interpret and integrate molecular cues to build complex structures like the face and peripheral nervous system. We use avian embryos (chicken, quail, and peafowl) and axolotls as powerful comparative models to ask fundamental questions about how cell identity and behavior are established and reshaped during embryogenesis:
- How do cells know what to become? Are these decisions controlled at multiple levels- from DNA to RNA to Protein?
- How do cells stay connected or let go? What molecular mechanisms regulate cell adhesion as some cells migrate while others remain in place?
- What makes one cell unique? How do differences in gene and protein expression define cellular individuality within and across species?
- What molecules are truly essential? How do specific proteins shape the choreography of development?
To answer these questions, we study the neural tube and neural crest, two closely related ectodermal cell populations that give rise to the central and peripheral nervous systems. We aim to uncover what distinguishes neural crest cells, the population that breaks away and migrates, from their neural progenitor neighbors that remain in the tube. This transformation, known as the epithelial-to-mesenchymal transition (EMT), is a striking example of how developmental programs drive dynamic changes in cell adhesion, shape, and identity.
We hypothesize that precise spatial and quantitative control of transcriptional regulators, adhesion molecules, and cytoskeletal dynamics enables this complex process.
Our current projects investigate:
Current Funding Sources:
1. NSF CAREER Grant , Functional Analysis of Crest EffectorS (FACES), 2143217 (2022-2026)
2. ASCB/MBL PAIR-UP Pilot Grant, Metadevices for longitudinal imaging of mitochondrial trafficking in peripheral nerves (8/01/23-07/31/26)
3. UC Davis Center for Companion Animal Health (2025-2026)
4. Hypothesis Fund (2025-2026)
In the Rogers Lab, we explore the molecular logic that guides cell fate decisions, morphogenesis, and migration during early vertebrate development. Our work focuses on uncovering how cells interpret and integrate molecular cues to build complex structures like the face and peripheral nervous system. We use avian embryos (chicken, quail, and peafowl) and axolotls as powerful comparative models to ask fundamental questions about how cell identity and behavior are established and reshaped during embryogenesis:
- How do cells know what to become? Are these decisions controlled at multiple levels- from DNA to RNA to Protein?
- How do cells stay connected or let go? What molecular mechanisms regulate cell adhesion as some cells migrate while others remain in place?
- What makes one cell unique? How do differences in gene and protein expression define cellular individuality within and across species?
- What molecules are truly essential? How do specific proteins shape the choreography of development?
To answer these questions, we study the neural tube and neural crest, two closely related ectodermal cell populations that give rise to the central and peripheral nervous systems. We aim to uncover what distinguishes neural crest cells, the population that breaks away and migrates, from their neural progenitor neighbors that remain in the tube. This transformation, known as the epithelial-to-mesenchymal transition (EMT), is a striking example of how developmental programs drive dynamic changes in cell adhesion, shape, and identity.
We hypothesize that precise spatial and quantitative control of transcriptional regulators, adhesion molecules, and cytoskeletal dynamics enables this complex process.
Our current projects investigate:
- Molecular control of cell fate and EMT: Characterizing the roles of transcription factors, adhesion proteins, and cytoskeletal components in neural crest specification and migration, and identifying their novel targets and cofactors.
- Cadherin dynamics: Defining the timing, regulation, and function of cadherin proteins during neural crest EMT and lineage commitment.
- Cell cycle and differentiation: Exploring how cadherin modulation influences proliferation and differentiation of neural crest-derived cells.
- Environmental disruptions: Investigating how exposure to teratogens perturbs normal embryonic development, revealing vulnerabilities in neural crest-driven morphogenesis.
Current Funding Sources:
1. NSF CAREER Grant , Functional Analysis of Crest EffectorS (FACES), 2143217 (2022-2026)
2. ASCB/MBL PAIR-UP Pilot Grant, Metadevices for longitudinal imaging of mitochondrial trafficking in peripheral nerves (8/01/23-07/31/26)
3. UC Davis Center for Companion Animal Health (2025-2026)
4. Hypothesis Fund (2025-2026)
|
|
|
|
|
|
The movies below are from an upcoming publication by Camilo V. Echeverria, Jr., et al., 2025. Images acquired on a Zeiss Lightsheet 7 at the UC Davis Advanced Imaging Facility.
|
|
The videos below are from a past publication: Sip1 mediates an E-cadherin-to-N-cadherin switch during cranial neural crest EMT. JCB. C.D. Rogers, A. Saxena, M.E. Bronner. December 2, 2013. doi: 10.1083/jcb.201305050.
|
This video depicts a normal avian embryo. The green cells are cranial neural crest cells (injected with a control morpholino) migrating laterally away from the neural tube.
This video depicts an avian embryo lacking Sip1. The green cells are cranial neural crest cells (injected with a translation blocking Sip1 morpholino). These cells have completed the first phase of EMT (detaching from the neural tube), but are unable to complete EMT and separate from each other.
|
This video depicts a normal avian embryo. The green cells are cranial neural crest cells (injected with a control morpholino and membrane RFP) migrating laterally away from the neural tube.
This video depicts an avian embryo lacking Sip1. The green cells are cranial neural crest cells (injected with a translation blocking Sip1 morpholino and membrane RFP). These cells have completed the first phase of EMT (detaching from the neural tube), but are unable to complete EMT and separate from each other.
|
