Kafatos:Povelones, Michael

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Michael Povelones   Division of Cell & Molecular Biology Imperial College South Kensington Campus SAF Building London, SW7 2AZ United Kingdom

Education BA in Chemistry, Columbia University, New York, NY, USA PhD in Developmental Biology, Stanford University, Stanford, CA, USA Biology of Parasitism 2005, MBL, Woods Hole, MA

Current Research Interests I am a postdoctoral fellow in the Kafatos/Christophides Lab at Imperial College, London. Science is cool.

Previous Research I received my doctoral degree at Stanford University in the laboratory of Roel Nusse. The focus of my research was understanding how the frizzled (fz) receptor in Drosophila functions in planar cell polarization (PCP) and Wnt-mediated cell fate specification. fz controls two different signal transduction pathways for each of these distinct developmental outcomes. How does a single receptor function in two signaling pathways? This work revealed that even though cell fate signaling requires a Wnt ligand, fz is not activated by any of the 7 Drosophila Wnt genes for its PCP function. Instead, fz has an intrinsic ability to control components of the PCP pathway and that it associates with pathway specific Wnt co-receptor for cell fate signaling. In addition, a structure-function analysis of fz suggested that, in addition to the Wnt binding site located in the extracellular cysteine-rich domain, there is a second Wnt-binding site within the transmembrane portion of the receptor. Povelones M and Nusse R. The role of the cysteine-rich domain of Frizzled in Wingless-Armadillo signaling. EMBO J 2005 Oct 5; 24(19) 3493-503. genetics2005 pmid=16085697 naturecellbio2002 pmid=12415278 I worked in the laboratory of Richard Ambron as an undergraduate and research technician at Columbia University. The focus of this research was the identification of intrinsic nerve injury signals. In addition to growth factor and electrophysiological responses, neurons posses axonal proteins with a masked nuclear localization sequence (NLS) that serve as a sensor for injury. These injury signals are activated and rapidly retrogradely transported to the neuronal cell body and into the nucleus following nerve crush injury. In the nucleus they function to initiate the transcriptional program for repair. My research focused on the identification of an NF-κB-like transcription factor in Aplysia and its function in nerve injury. Nerve regeneration following injury requires transcriptional activation of repair genes. Members NF-κB family of transcription factors are well-suited to play a role in nerve injury since they contain and masked NLS and are localized to the cytoplasm until activated. This work identified by electrophoretic mobility shift assay an NF-κB-like activity in axoplasm. Contrary to what was expected, this activity was rapidly inactivated in injured neurons. We hypothesized that in these neurons, NF-κB functions as a signal of homeostasis and must be inactivated following injury since it regulates genes that are incompatible with repair. Sung YJ, Povelones M, and Ambron RT. RISK-1: a novel MAPK homologue in axoplasm that is activated and retrogradely transported after nerve injury. J Neurobiol. 2001 Apr;47(1):67-79. DOI:10.1002/neu.1016 | Farr M, Zhu DF, Povelones M, Valcich D, and Ambron RT. Direct interactions between immunocytes and neurons after axotomy in Aplysia. J Neurobiol. 2001 Feb 5;46(2):89-96. Povelones M, Tran K, Thanos D, and Ambron RT. An NF-kappaB-like transcription factor in axoplasm is rapidly inactivated after nerve injury in Aplysia. J Neurosci. 1997 Jul 1;17(13):4915-20. DOI:10.1523/JNEUROSCI.17-13-04915.1997 | Ambron RT, Zhang XP, Gunstream JD, Povelones M, and Walters ET. Intrinsic injury signals enhance growth, survival, and excitability of Aplysia neurons. J Neurosci. 1996 Dec 1;16(23):7469-77. DOI:10.1523/JNEUROSCI.16-23-07469.1996 |