Current Lab Members
Emily Bates, Principal Investigator
We use mutations that are found in human patients to give us clues into the basic biology that underlies normal development. For example, mutations in ion channels cause syndromes of birth defects. We made similar mutations in fruit flies and mice to discover that ion channels are important for bone morphogenic protein signaling and morphological development. These studies have led us to the hypothesis that substances that affect ion channel function (such as nicotine and marijuana components) could impact fetal development. We are particularly interested in how cannabidiol (CBD) impacts exposure impacts fetal development in mice. A second project focuses on how microtubules are regulated for axon outgrowth and neuronal migration for brain development.
Outside the lab, I like to play with my kids, run, ski, hike, and play violin.
Karli Swenson, PhD Candidate
Research Project: Marijuana for Morning Sickness: Defining the impact of CBD exposure on fetal brain development and postnatal behavior
Morning sickness is debilitating for hundreds of thousands of pregnant people each year. To help reduce pregnancy nausea and vomiting, many pregnant people choose to consume marijuana, or one of its components cannabidiol (CBD). While clinical studies of marijuana consumption during pregnancy show impacts to baby's brain development or behavior, these studies don't delineate the role of CBD specifically. In my thesis, I am administering CBD to pregnant mice and analyzing the brain development and behavior of the offspring. In addition to characterizing the impact of CBD exposure alone, I am also investigating the role of a CBD target called the Transient Receptors Potential Villanoid 1 (TRPV1) channel.
Outside of lab, I love to backpack, take film photos, and try new sushi restaurants.
Twitter, Instagram, Website
Kyle Northington, PhD Candidate
Outside of lab, I like cooking, going to the movies, and snowboarding.
Emily Fontenoy, Professional Research Assistant
Research Project: The role of ion channels in Drosophila melanogaster development.
I am investigating the role that ion channels play in development using the Drosophila wing as a model. The Drosophila wing is sensitive to changes in developmental pathways and previous research in the lab as identified 46 ion channels that cause wing defects when disrupted. Five of the 46 ion channels, SERCA, Best2, Stim, SK, and Orai, are needed for tight regulation of endoplasmic reticulum (ER) calcium. Because the defects that wing specific knockdowns of these ion channels produce are like the defects seen when there are disruptions of the BMP homolog Dpp, I am focusing on the impact that disruptions in these ER-calcium regulating channels have on the Dpp pathway in Drosophila wing development.
Outside the lab I like knitting and reading.
Laura George, PhD (Graduated 2021)
Research Project: The role of Ion channels in development through Drosophila melanogaster
In my project I am investigating the role of ion channels in development using Drosophila melanogaster. The Drosophila wing is acutely sensitive to changes in developmental pathways, and in a screen of ion channels expressed in the wing we have identified 57 ion channels that cause wing defects when disrupted. I am investigating the developmental pathways that these ion channels impact and the mechanisms by which they impinge upon these pathways.
Outside of the lab I enjoy hiking, running, reading, photography, and playing the harp.
Most recent publication: Ion Channel Contributions to Wing Development in Drosophila melanogaster.
Georgia Buscaglia, PhD (Graduated 2020)
Research project: Elucidating the role of a brain specific tubulin, Tuba1a in neuronal function and development.
In neurons, the microtubule cytoskeleton supports the formation of elaborate neuronal morphologies, facilitates axon pathfinding and synapse formation, and allows for intracellular trafficking. The alpha tubulin gene, TUBA1A, encodes the most highly expressed alpha tubulin protein in the brain. TUBA1A is expressed in developing post-mitotic neurons, and mutations to this gene in humans result in severe developmental brain malformations, called tubulinopathies. We showed that an Asparagine to Aspartic acid substitution at residue 102 (Tuba1aN102D) results in severe brain malformations and perinatal death in mice that are homozygous for this mutation. Recently we have shown that mice heterozygous for this mutation (Tuba1aN102D/+) display more subtle disruption of brain development, specifically impairing axon pathfinding through large brain commissures. Additionally, Tuba1aN102D/+ mice develop an adult-onset behavioral motor deficit, that is not accompanied by neuronal cell death. Thus, we are using the Tuba1aN102D allele to interrogate the role that TUBA1A plays in neuronal microtubule function, in the context of both brain development and aging.
Jayne Aiken, PhD (Graduated 2019)
Research Project: Using Tubulinopathy patient mutations to understand how microtubules contribute to neuronal architecture and brain development.
My thesis work focuses on unveiling the mechanism underlying brain malformations found in patients harboring mutations in their tubulin genes. My research questions have lead me to learn and employ numerous model systems including in utero electroporation to discern if the patient-derived mutations dominantly alter neuronal migration, in vitro rat primary cortical neurons to assess cellular morphology, and budding yeast to investigate how patient mutations impact the function of tubulin proteins. This research has provided valuable insight into the mechanism behind the most common α-tubulin variant associated with disease, TUBA1A-R402C/H, revealing that it disrupts association with an important microtubule motor, dynein, and that the level of disruption scales with mutant abundance in the cell. This work provides the essential molecular link from mutation to the harmful brain malformation.
Most recent publication: TUBA1A mutations identified in lissencephaly patients dominantly disrupt neuronal migration and impair dynein activity.
Trevor Isner, PRA
Currently a PhD student in the Barlow Lab on campus
Research Project: Ion channels in morphological development
The project I am working on primarily focuses on studying the underlying mechanisms driving diseases like Anderson-Tawil syndrome and how specific ion channels play a role in development. By investigating mutations that occur within the ion channel Kir2.1, I am hoping to elucidate some of the mystery behind how ion channels and signaling proteins like BMP and Wnt work together to result in the phenotypes seen in patients with these syndromes. Using mice as a model organism combined with prior research done in Drosophila melanogaster, we can then apply these findings to human patients. Outside of the lab I enjoy activities like hiking, snowboarding, playing guitar and caring for my own model organisms (cats and axolotls).
Giri Dahal, PhD
Publications associated with the Bates Lab: