524 Poster abstracts / Int. J. Devl Neuroscience 24 (2006) 495–603 [P65] Identifying synapse formation genes regulated by a presy- naptic E3 ubiquitin ligase E. Liao * , W. Hung, M. Zhen Samuel Lunenfeld Research Institute, Canada The neuronal synapse is an asymmetric structure consisting of pre and post-synaptic terminals in direct apposition. Synapse formation is a highly regulated process requiring the interac- tion of many genetic pathways. To identifying genes that are required for the proper formation of synapses we are using the GABAergic nervous system of C. elegans as our model system. C. elegans is an excellent model system due to its strong genetics and characterized and invariant nervous system. Fluorescently tagged synaptic proteins allow for the visualization of synapses in live animals and thus the identification of synapse mutants through genetic screens. We have identified a protein complex that controls synapse morphology. This SCF ubiquitin ligase complex consists of the F-box protein FSN-1, the RING finger protein RPM-1, Skp1, and Cullin. This complex is required pre-synaptically and is localized to the peri-active zone. We hypothesize that this pro- tein complex controls synapse formation by down regulating synapse-promoting factors through an ubiquitin mediated pro- cess. We have identified a possible target or downstream effector of synapse formation in the receptor protein tyrosine kinase scd- 2 (suppressor of constitutive dauer). We have observed that protein levels of an SCD-2::GFP fusion protein increase in the absence of fsn-1 in vivo. SCD- 2 ubiquitination is currently being tested. We have shown that loss of scd-2 will partially rescue the synapse defects of fsn- 1 and rpm-1, and suppression of fsn-1 defects is specific for alleles of scd-2 that are defective in the C-terminal kinase. The incomplete suppression of fsn-1 by scd-2 suggests the existence of other pathways regulated by fsn-1. We are in the process of identifying other components of signaling pathways through which fsn-1 regulates synapse morphology. Keywords: Synapse; Ubiquitin; fsn-1; C. elegans doi:10.1016/j.ijdevneu.2006.09.128 [P67] Cell fate specification and axonogenesis in neurons fate mapped from the embryonic rhombic lip R. Machold * , C. Klein, G. Fishell NYU Medical Center, USA The cerebellum develops from an embryonic primordium within dorsal rhombomere 1 (r1) that contains two germi- nal zones: the ventricular neuroepithelium and the cerebel- lar rhombic lip. Specification of neurons in the rhombic lip requires the basic helix–loop–helix (bHLH) transcription factor Math1, a mouse homolog of Drosophila atonal. Recently, we have fate mapped the cerebellar rhombic lip using an in vivo inducible cre/loxP recombination strategy (Math1-CreER T2 ; R26RstopLacZ) to permanently label cohorts of Math1 + cells at early and late embryonic stages. At stages prior to E12.5, with the exception of the deep cerebellar nuclei, we find that Math1 + rhombic lip neurons migrate out of the cerebellar primordium into the rostral hindbrain to populate specific nuclei that include cholinergic neurons of the mesopontine tegmental system. Inter- estingly, many of these hindbrain nuclei are components of the auditory and vestibular systems, suggesting that Math1 expres- sion may impart a circuit identity on pools of rhombic lip neural progenitors. We will present new data from a microarray analy- sis of the Math1 populations generated in the cerebellar rhombic lip between E11.5 and E13.5 we performed to characterize the genes expressed downstream of Math1 that direct the differ- entiation of these populations. Furthermore, using a recently developed reporter line that expresses membrane targeted GFP, we have begun to characterize the formation of axonal projec- tions between Math1-derived nuclei, as well as other projections to the rostral CNS. We will present this data along with expres- sion data for candidate cell surface molecules that may mediate the specific projection patterns observed in the embryonic devel- opment of these neural circuits. Keywords: Cell fate specification; Axonogenesis; Math1; Hind- brain development doi:10.1016/j.ijdevneu.2006.09.129 [P68] Cacna1f-mutant mouse exhibits altered synaptogenesis N. Orton * , W.K. Stell, T. Bech-Hansen University of Calgary, Canada Introduction: Mutations in CACNA1F, which encodes the human Ca v 1.4 subunit of an L-type voltage-gated calcium chan- nel, cause incomplete Congenital Stationary Night Blindness (CSNB2). This highly variable X-linked retinal disorder is characterized by night blindness, reduced visual acuity, and an abnormal electrophysiological response in addition to sec- ondary visual impairments. Recently we reported pronounced morphological changes in second-order neurons of the retina of a transgenic model of CSNB2 (Anon., 2005): ON-bipolar and horizontal cell processes extended distally from the outer plex- iform layer, deep into the outer nuclear layer (ONL). Key pre- and post-synaptic components: bassoon, ribeye, and mGluR6 occurred only rarely in their normal location in the OPL or even ectopically in the ONL. This suggested that photoreceptor synapses either fail to develop properly, or degenerate after being formed, in the mutant retina. In the present study we attempted to distinguish between these two alternatives. Methods: We used transmission electron microscopy and immunocytochemistry to study the retinas from a mouse model of CSNB2, G305X, which we generated by targeted disruption