The C-terminal motif is not completely conserved in GCGR

amined by time-lapse imaging. We found that the rate of filopodial assembly was suppressed under the influence of these two receptor constructs, much as in our recent study showing that a mutant form of p120 catenin that fails to inhibit RhoA blocks the initiation of new filopodia. Because axonal filopodial formation and outgrowth are both processes that depend on membrane addition, we tested whether FGFR1 and TrkB also affect the rate of axonal advance differently. Compared to control neurons, neurons expressing WT-FGFR1 or TR-TrkB grew 4060 % slower while those expressing TR-FGFR1 or WT-TrkB grew,50 % faster, suggesting that inhibition of FGFR1 or activation of TrkB promoted neuronal growth and activation of FGFR1 or inhibition of TrkB impeded growth. Thus, FGFR1 and TrkB oppositely regulated filopodial assembly as well as axonal growth in neurons. Influence of TrkB and FGFR1 on filopodial extension by neurons towards muscle Xenopus spinal neurons approaching muscle cells extend more 487-52-5 filopodia from their muscle-facing side than from the opposite side, indicating that these filopodia are induced by factors presented by muscle, such as bFGF. To investigate how TrkB regulates muscle-dependent filopodial extension by neurons, spinal neurons expressing GFP, WT-TrkB or TR-TrkB were cocultured with 7d-old muscle cells. The growth of neuronal filopodia towards muscle cells was quantified as asymmetry index values using nerve-muscle pairs as previously described. Neurons expressing WT-TrkB extended filopodia less preferentially towards muscle than GFP-neurons, suggesting that the activation of TrkB not only reduced the spontaneous formation of filopodia but also inhibited the induction of neuronal filopodia by muscle. In contrast, neurons expressing TR-TrkB retained the ability to grow more filopodia towards muscle cells than away from them. Next we examined the behavior of neurons expressing exogenous TrkB proteins when they approached muscle cells overexpressing bFGF. In this experiment, muscle cells isolated FGF and TrkB Receptor Signaling in NMJ Development The transparent and refractive cornea plays a central role in vision. Abnormal development and/or maintenance of the cornea result in severe defects in vision. Molecular and cellular events involved in corneal development, maturation and maintenance have been studied in great detail. Members of different transcription factor families including Kruppel-like factors influence corneal morphogenesis. More than 17 members of the KLF family have been identified in mammals, many of which are expressed in the ocular surface in varying amounts. Among them, structurally related Klf4 and Klf5 are two of the most highly expressed transcription factors in the mouse cornea. Our previous studies demonstrated that both Klf4 and Klf5 are essential for normal maturation and maintenance of the mouse ocular surface. 1 Corneal Klf5-Target Genes Klf4 and Klf5 exert tissue-dependent and non-redundant influences on the mouse ocular surface in spite of possessing an identical DNA-binding domain. Conditional disruption of Klf4 in the developing mouse ocular surface resulted in numerous defects including corneal epithelial fragility, stromal edema, altered stromal collagen fibril organization, endothelial vacuolation and loss of mucin producing conjunctival goblet cells. Similar conditional disruption of Klf5 also resulted in multiple defects including translucent cornea, abnormal eyelids with malformed meibomian