Kafatos:Povelones, Michael: Difference between revisions
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==Previous Research== | ==Previous Research== | ||
[[Image:Kafatos-pove-fz.png|thumb|right|100px|Frizzled is cool]] | |||
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. | 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. | ||
Revision as of 13:17, 19 August 2006
Michael Povelones Division of Cell & Molecular Biology |
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.
Publications
- 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. DOI:10.1038/sj.emboj.7600817 |
- Povelones M, Howes R, Fish M, and Nusse R. Genetic evidence that Drosophila frizzled controls planar cell polarity and Armadillo signaling by a common mechanism. Genetics. 2005 Dec;171(4):1643-54. DOI:10.1534/genetics.105.045245 |
- Povelones M and Nusse R. Wnt signalling sees spots. Nat Cell Biol. 2002 Nov;4(11):E249-50. DOI:10.1038/ncb1102-e249 |
- 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 |