Research Interests
I am interested in basic developmental biology research as the basis of understanding for both discovering therapies and cures for congenital disorders and repairing or preventing adult disease. I want to continue to make this important field understandable and accessible for young researchers by continuing to develop my skills for meaningful research while working with model organisms that can be adapted for young scientists.
My work currently uses Drosophila (fruit flies) and zebrafish to study the genes and transcription factors important in regulating both cardiac and skeletal muscle developmental processes.
Potential projects for undergraduate study:
I am interested in basic developmental biology research as the basis of understanding for both discovering therapies and cures for congenital disorders and repairing or preventing adult disease. I want to continue to make this important field understandable and accessible for young researchers by continuing to develop my skills for meaningful research while working with model organisms that can be adapted for young scientists.
My work currently uses Drosophila (fruit flies) and zebrafish to study the genes and transcription factors important in regulating both cardiac and skeletal muscle developmental processes.
Potential projects for undergraduate study:
- miRNAs in muscle development and maintenance
- Vertebrate orthologs of muscle associated genes
- Muscle cell type specification development
Post-Doctoral Research
As a post-doctoral researcher in Dr. Richard Cripps' laboratory, I am focusing on a few projects. My early projects characterized newly generated mutant Drosophila lines for Actin57B and Actin79B. Actin57B is the predominant actin in embryos while Actin79B is found in adult jump muscles. These actin mutants are allowing us interesting insights into muscle development and the redundancy of similar actin genes.
Another project I am pursuing in the lab involved the role of MRTF in early muscle development. MRTF is know to have roles in smooth muscle development and cardiac development and repair. Research in our lab has identified a role for MRTF and its binding partner SRF (Drosophila blistered) in skeletal muscle development. I am continuing this project looking at early cell autonomous roles for MRTF in skeletal muscle development.
I also have the opportunity to mentor three undergraduate students in the Cripps lab. Mr. Paudel is currently working on a project to characterize the effects of a hyperactive and dominant negative form of MRTF in adult Drosophila muscle development. Mr. Wilson is currently working on a project looking at the role of miRNAs in skeletal muscle development. Ms. Garay worked with us one summer as part of the UPN summer research program at UNM. Ms Garay's project involved looking for zebrafish orthologs of Drosophila genes and identifying potential muscle program regulators.
As a post-doctoral researcher in Dr. Richard Cripps' laboratory, I am focusing on a few projects. My early projects characterized newly generated mutant Drosophila lines for Actin57B and Actin79B. Actin57B is the predominant actin in embryos while Actin79B is found in adult jump muscles. These actin mutants are allowing us interesting insights into muscle development and the redundancy of similar actin genes.
Another project I am pursuing in the lab involved the role of MRTF in early muscle development. MRTF is know to have roles in smooth muscle development and cardiac development and repair. Research in our lab has identified a role for MRTF and its binding partner SRF (Drosophila blistered) in skeletal muscle development. I am continuing this project looking at early cell autonomous roles for MRTF in skeletal muscle development.
I also have the opportunity to mentor three undergraduate students in the Cripps lab. Mr. Paudel is currently working on a project to characterize the effects of a hyperactive and dominant negative form of MRTF in adult Drosophila muscle development. Mr. Wilson is currently working on a project looking at the role of miRNAs in skeletal muscle development. Ms. Garay worked with us one summer as part of the UPN summer research program at UNM. Ms Garay's project involved looking for zebrafish orthologs of Drosophila genes and identifying potential muscle program regulators.
Graduate Research
During my graduate research I focused on two main projects looking at early stages of cardiac development in zebrafish embryos. The first project involved using heat-shock inducible genes to regulate Wnt signaling in the zebrafish embryo. This allowed us to determine temporal requirements for Wnt signaling throughout early development. Along with the known roles of Wnt signaling in promoting mesoderm induction and later restricting ventricular cardiomyocyte proliferation, we were able to show that Wnt signaling is sufficient to inhibit cardiac differentiation during early somitogenesis resulting in specified cardiac progenitors dying through a p53 independent pathway, as well as a novel role in atrial cell differentiation during late somitogenesis. This project also allowed collaboration with anther project in the lab looking at the downstream component of the Wnt signaling pathway, Lef/Tcf proteins. Through comparison of Wnt loss of function (morphant) embryos and Lef loss of function (morphant) embryos we were able to determine overlapping and specific roles for Lef proteins in zebrafish cardiac development.
My second graduate project involved looking at genes downstream of retinoic acid signaling, specifically genes that might be involved in cardiac development. Retinoic acid signaling is known to restrict the cardiac field leading to an appropriately sized heart. The lab identified the gene nr2f1a as being downstream of retinoic acid signaling. I confirmed that nr2f1a is downstream of retinoic acid signaling and was able to detect a putative retinoic acid binding site in the nr2f1a promoter region through EMSA and ChIP experiments. Further, I was able to demonstrate a role for nr2f1a in limiting the ventricular chamber of the heart during early development through established techniques looking at progenitor and cardiac cell numbers and expression levels. Interestingly, this restriction of the cardiac field appears to work in conjunction with the promotion of the pharyngeal mesoderm and later jaw and neck muscle development. This was initially observed in loss of function (morphant) embryos and later confirmed in mutant zebrafish embryos. This was the first signaling pathway to be implicated in the fate decision of progenitor cells to become ventricular cardiomyocytes or pharyngeal mesoderm.
During my graduate student rotations, I was also given the opportunity to work with Xenopus embryos to determine regulatory elements in the hex gene promoter region that confine hex expression to the developing endoderm mentored by Dr. Aaron Zorn. Another rotation allowed me to work with developing a mouse model for atopic dermatitis and potential signaling pathways that could be manipulated to promote skin healing after injury under the direction of Dr. Gurjit Hershey.
During my graduate research I focused on two main projects looking at early stages of cardiac development in zebrafish embryos. The first project involved using heat-shock inducible genes to regulate Wnt signaling in the zebrafish embryo. This allowed us to determine temporal requirements for Wnt signaling throughout early development. Along with the known roles of Wnt signaling in promoting mesoderm induction and later restricting ventricular cardiomyocyte proliferation, we were able to show that Wnt signaling is sufficient to inhibit cardiac differentiation during early somitogenesis resulting in specified cardiac progenitors dying through a p53 independent pathway, as well as a novel role in atrial cell differentiation during late somitogenesis. This project also allowed collaboration with anther project in the lab looking at the downstream component of the Wnt signaling pathway, Lef/Tcf proteins. Through comparison of Wnt loss of function (morphant) embryos and Lef loss of function (morphant) embryos we were able to determine overlapping and specific roles for Lef proteins in zebrafish cardiac development.
My second graduate project involved looking at genes downstream of retinoic acid signaling, specifically genes that might be involved in cardiac development. Retinoic acid signaling is known to restrict the cardiac field leading to an appropriately sized heart. The lab identified the gene nr2f1a as being downstream of retinoic acid signaling. I confirmed that nr2f1a is downstream of retinoic acid signaling and was able to detect a putative retinoic acid binding site in the nr2f1a promoter region through EMSA and ChIP experiments. Further, I was able to demonstrate a role for nr2f1a in limiting the ventricular chamber of the heart during early development through established techniques looking at progenitor and cardiac cell numbers and expression levels. Interestingly, this restriction of the cardiac field appears to work in conjunction with the promotion of the pharyngeal mesoderm and later jaw and neck muscle development. This was initially observed in loss of function (morphant) embryos and later confirmed in mutant zebrafish embryos. This was the first signaling pathway to be implicated in the fate decision of progenitor cells to become ventricular cardiomyocytes or pharyngeal mesoderm.
During my graduate student rotations, I was also given the opportunity to work with Xenopus embryos to determine regulatory elements in the hex gene promoter region that confine hex expression to the developing endoderm mentored by Dr. Aaron Zorn. Another rotation allowed me to work with developing a mouse model for atopic dermatitis and potential signaling pathways that could be manipulated to promote skin healing after injury under the direction of Dr. Gurjit Hershey.
Undergraduate Research
My undergraduate honors thesis observed zebrafish development to determine signaling molecules regulating the axon guidance of motor neurons. Under the direction of Dr. Michelle McWhorter I was able to use loss of function (morphant) embryos to disrupt plexinb1b expression in early zebrafish embryos. This decrease in plexinb1b caused motor neuron axons to become truncated before they reached the muscle, or to create multiple branches, many of which never reached the muscle indicating the key role of plexinb1b in motor neuron axon guidance.
I also had the opportunity in my undergraduate career to do field work in The Bahamas, looking at microhabitat selection of two tropical snail species Nerita versicolor and N. peloronta under the direction of Dr. Timothy Lewis.
My undergraduate honors thesis observed zebrafish development to determine signaling molecules regulating the axon guidance of motor neurons. Under the direction of Dr. Michelle McWhorter I was able to use loss of function (morphant) embryos to disrupt plexinb1b expression in early zebrafish embryos. This decrease in plexinb1b caused motor neuron axons to become truncated before they reached the muscle, or to create multiple branches, many of which never reached the muscle indicating the key role of plexinb1b in motor neuron axon guidance.
I also had the opportunity in my undergraduate career to do field work in The Bahamas, looking at microhabitat selection of two tropical snail species Nerita versicolor and N. peloronta under the direction of Dr. Timothy Lewis.