This mechanism is robust because each of these

TRNs is ef

This mechanism is robust because each of these

TRNs is effectively transformed into a functional PVD-like neuron when either ahr-1 or zag-1 is genetically eliminated ( Figures 2, 4, 5, and S3). Thus, our work has revealed the logic of alternative genetic regulatory pathways in which a single type of transcription factor (e.g., MEC-3) can specify the differentiation of two distinct classes of mechanosensory neurons ( Figure 8G). A related mechanism accounts in part for the dose-dependent effects of the homeodomain transcription factor Cut on the branching complexity of larval sensory neurons in Drosophila ( Grueber et al., 2003). The transcription factor Knot/Collier is selectively deployed in Type IV da neurons to antagonize expression of Cut targets that produce the dendritic spikes that selleck products are characteristic of Type III da neurons. In this case, however, Knot does not regulate Cut expression but functions in a parallel pathway ( Jinushi-Nakao et al., 2007). Our finding that the Zinc-finger transcription factor ZAG-1 is required to prevent the PVM touch neuron from adopting

a PVD nociceptor fate mirrors the recent observation that genetic ablation of the mammalian ZAG-1 homolog Zfhx1b (Sip1, Zeb2) results in cortical interneurons adopting the fate of striatal GABAerigic cells ( McKinsey et al., 2013). Our results are suggestive of a potentially complex regulatory mechanism in which AHR-1 and ZAG-1 inhibit expression of nociceptor genes (e.g., hpo-30) whereas MEC-3 activates transcription of these targets. Additional upstream regulators of mec-3, UNC-86, and ALR-1, are also likely involved in this pathway ( Topalidou Ivacaftor research buy et al., 2011 and Xue et al., 1992). Although transcription factors see more are well-established determinants of sensory neuron fate, the downstream pathways that they regulate are largely unknown (Jan and Jan, 2010,

Jinushi-Nakao et al., 2007, Parrish et al., 2006 and Sulkowski et al., 2011). As a solution to this problem for MEC-3, we used a cell-specific profiling strategy (Petersen et al., 2011, Spencer et al., 2011 and Von Stetina et al., 2007) to detect mec-3-regulated transcripts in the PVD neuron. We used a combination of RNAi and mutant analysis to identify the subset of targets that affect PVD branching morphogenesis ( Figure S6; Tables S3 and S5). Additional experiments with one of these hits, the claudin-like protein HPO-30, revealed a key role in the generation of PVD branches. We note that HPO-30 is expressed in the FLP neuron ( Figure S7), where it also mediates the higher order branching morphology shared by FLP and PVD ( Smith et al., 2010 and Topalidou and Chalfie, 2011) ( Figure S7). Time-lapse imaging has revealed that PVD lateral or 2° branches may adopt either of two different modes of outgrowth along the inside surface of the epidermis: (1) fasciculation with existing motor neuron commissures or (2) independent extension as noncommissural or “pioneer” dendrites ( Smith et al.

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