Education
- PhD, 1994, Baylor College of Medicine; MD, 1997, Baylor College of Medicine
- BS, 1989, Biochemistry, Louisiana State University
Research Summary
Using Drosophila, we study how neurons form synaptic connections, as well as how synapses transmit information and change during learning and memory. We also investigate how alterations in neuronal signaling underlie several neurological diseases, including epilepsy, autism, and Huntington’s Disease. We hope to bridge the gap between the molecular components of the synapse and the physiological responses they mediate.Key Publications
- A synaptotagmin suppressor screen indicates SNARE binding controls the timing and Ca2+ cooperativity of vesicle fusion. Guan, Z, Bykhovskaia, M, Jorquera, RA, Sutton, RB, Akbergenova, Y, Littleton, JT. 2017. Elife 6, .
doi: 10.7554/eLife.28409PMID:28895532 - Phosphorylation of Complexin by PKA Regulates Activity-Dependent Spontaneous Neurotransmitter Release and Structural Synaptic Plasticity. Cho, RW, Buhl, LK, Volfson, D, Tran, A, Li, F, Akbergenova, Y, Littleton, JT. 2015. Neuron 88, 749-61.
doi: 10.1016/j.neuron.2015.10.011PMID:26590346 - Spontaneous and evoked release are independently regulated at individual active zones. Melom, JE, Akbergenova, Y, Gavornik, JP, Littleton, JT. 2013. J. Neurosci. 33, 17253-63.
doi: 10.1523/JNEUROSCI.3334-13.2013PMID:24174659 - A complexin fusion clamp regulates spontaneous neurotransmitter release and synaptic growth. Huntwork, S, Littleton, JT. 2007. Nat. Neurosci. 10, 1235-7.
doi: 10.1038/nn1980PMID:17873870 - Retrograde signaling by Syt 4 induces presynaptic release and synapse-specific growth. Yoshihara, M, Adolfsen, B, Galle, KT, Littleton, JT. 2005. Science 310, 858-63.
doi: 10.1126/science.1117541PMID:16272123
Recent Publications
- Glial Ca2+signaling links endocytosis to K+ buffering around neuronal somas to regulate excitability. Weiss, S, Melom, JE, Ormerod, KG, Zhang, YV, Littleton, JT. 2019. Elife 8, .
doi: 10.7554/eLife.44186PMID:31025939 - Neurons regulate synaptic strength through homeostatic scaling of active zones. Cunningham, KL, Littleton, JT. 2019. J. Cell Biol. 218, 1434-1435.
doi: 10.1083/jcb.201903065PMID:30979798 - Characterization of developmental and molecular factors underlying release heterogeneity at Drosophila synapses. Akbergenova, Y, Cunningham, KL, Zhang, YV, Weiss, S, Littleton, JT. 2018. Elife 7, .
doi: 10.7554/eLife.38268PMID:29989549 - A synaptotagmin suppressor screen indicates SNARE binding controls the timing and Ca2+ cooperativity of vesicle fusion. Guan, Z, Bykhovskaia, M, Jorquera, RA, Sutton, RB, Akbergenova, Y, Littleton, JT. 2017. Elife 6, .
doi: 10.7554/eLife.28409PMID:28895532 - Astrocyte Ca2+ Influx Negatively Regulates Neuronal Activity. Zhang, YV, Ormerod, KG, Littleton, JT. eNeuro 4, .
doi: 10.1523/ENEURO.0340-16.2017PMID:28303263 - Pathogenic Huntington Alters BMP Signaling and Synaptic Growth through Local Disruptions of Endosomal Compartments. Akbergenova, Y, Littleton, JT. 2017. J. Neurosci. 37, 3425-3439.
doi: 10.1523/JNEUROSCI.2752-16.2017PMID:28235896 - Neurotoxicity Pathways in Drosophila Models of the Polyglutamine Disorders. Krench, M, Littleton, JT. 2017. Curr. Top. Dev. Biol. 121, 201-223.
doi: 10.1016/bs.ctdb.2016.07.006PMID:28057300 - Characterization of axonal transport defects in Drosophila Huntingtin mutants. Weiss, KR, Littleton, JT. J. Neurogenet. 30, 212-221.
doi: 10.1080/01677063.2016.1202950PMID:27309588 - A Drosophila model of Huntington disease-like 2 exhibits nuclear toxicity and distinct pathogenic mechanisms from Huntington disease. Krench, M, Cho, RW, Littleton, JT. 2016. Hum. Mol. Genet. 25, 3164-3177.
doi: 10.1093/hmg/ddw166PMID:27288455 - Shank Modulates Postsynaptic Wnt Signaling to Regulate Synaptic Development. Harris, KP, Akbergenova, Y, Cho, RW, Baas-Thomas, MS, Littleton, JT. 2016. J. Neurosci. 36, 5820-32.
doi: 10.1523/JNEUROSCI.4279-15.2016PMID:27225771