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When citing an abstract from the 2009 Annual - Society for ...

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Time: Tuesday, October 20, <strong>2009</strong>, 8:00 am - 12:00 noon<br />

Program#/Poster#: 505.5/A5<br />

Topic: A.02.b. Cell lineage <strong>an</strong>d cell fate specification<br />

Support: CIHR<br />

HSFO<br />

Centre <strong>for</strong> Stroke Recovery<br />

OGS<br />

OGSST<br />

Title: Eip63E, <strong>the</strong> Drosophila PFTAIRE, is required <strong>for</strong> <strong>the</strong> proper development of <strong>the</strong> central<br />

nervous system<br />

Authors: *Y. RODRIGUEZ GONZALEZ 1 , P. JAFARNEJAD 3 , D. HAWARI 2 , R. S.<br />

SLACK 2 , M. SONNENFELD 2 , D. S. PARK 2 ;<br />

1 Dept Neurosci, 2 Cell. <strong>an</strong>d Mol. Med., Univ. of Ottawa, Ottawa, ON, C<strong>an</strong>ada; 3 Dept. of Mol. <strong>an</strong>d<br />

Hum<strong>an</strong> Genet., Baylor Col. of Med., Houston, TX<br />

Abstract: The characterization of <strong>the</strong> processes that control brain development is critical <strong>for</strong><br />

developing <strong>the</strong>rapeutic strategies that rely on accurate differentiation <strong>an</strong>d targeting events.<br />

PFTAIRE is a novel member of <strong>the</strong> growing number of Cyclin Dependent Kinases (CDK) that is<br />

normally resident in neurons. CDK5, <strong>the</strong> best characterized of neuronal CDKs, has been shown<br />

to participate in brain development <strong>an</strong>d death. Although PFTAIRE biological function <strong>an</strong>d<br />

regulation are hardly known, its expression in neurons <strong>an</strong>d similarity to CDK5 suggest a<br />

potentially import<strong>an</strong>t role in <strong>the</strong> CNS. Using two different Eip63E Drosophila mut<strong>an</strong>t lines, we<br />

show here that PFTAIRE mut<strong>an</strong>t flies display defects as early as stage 9 of embryonic<br />

development, as revealed by immunostaining <strong>for</strong> CNS markers such as engrailed/invected (4D9),<br />

neurogli<strong>an</strong> (BP104), repo (8D12), fasciclinII (1D4) <strong>an</strong>d BP102 <strong>an</strong>tigen. Results show that <strong>the</strong><br />

defects include at least a striking disorg<strong>an</strong>ization of neuronal <strong>an</strong>d glia cell bodies as well as<br />

abnormal arr<strong>an</strong>gements of both commissural <strong>an</strong>d longitudinal axons of <strong>the</strong> ventral nerve cord.<br />

Disclosures: Y. Rodriguez Gonzalez, None; P. JafarNejad, None; D. Hawari, None; R.S.<br />

Slack, None; M. Sonnenfeld, None; D.S. Park, None.<br />

Poster<br />

505. Cell Lineage <strong>an</strong>d Cell Fate Specification

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