Systems that regulate establishment, maintenance, and remodeling of dendritic fields. dendritic arbors is crucial for the ability of neurons to integrate information and sample the environment appropriately (Hall and Treinin, 2011). These arbors may vary greatly in shape and complexity, reflecting the different types of input they receive. Accordingly, loss of dendritic complexity and structure has been linked to a range of neurological conditions, including autism spectrum disorders, schizophrenia, and Alzheimers disease (Kaufmann and Moser, 2000; Kulkarni and Firestein, 2012). FX-11 Our understanding of dendrite morphogenesis in the sensory system has advanced significantly through the use of model organisms (reviewed in Jan and Jan, 2010). For instance, in (Oren-Suissa et al., 2010) and transcription factors (e.g., has been shown to act in PVD dendrites to promote PVD branching (Liu and Shen, 2012). Open in a separate window Figure 1 MNR-1 Is a Conserved Protein that Is Required for Development, but Not Maintenance, of Dendritic Arbors(A) Schematic of the PVD neuron in its tissue context. Primary (1), secondary (2), tertiary (3), and quaternary (4) dendritic branches are indicated. FX-11 hyp, hypodermis (skin). (B) Lateral view of an adult wild-type animal. PVD sensory neurons are visualized by a fluorescent reporter mutant animal. (D and E) Details of (B) and (C) as indicated. (F and G) Dorsal views of adult wild-type and mutant animals. FLP sensory neurons are visualized by a fluorescent reporter and (Figure S1 available online; Table S1; Experimental Procedures). Because of the fully FX-11 penetrant phenotype characterized by disorganization of the PVD dendritic menorahs, we named the gene mutants were characterized by disoriented growth of all higher-order PVD branches (secondary to quaternary), with many instances of crossovers, looping, and loss of orthogonality (Figures 1BC1E). Moreover, tiling of menorahs across the primary branch was severely impaired in these mutants, as was self-avoidance of sister branches (Figure 1). In contrast, the axon of PVD did not exhibit obvious guidance defects and we did not FX-11 detect defects in the viability, fertility, or locomotion of mutant animals (data not shown). Similar defects in dendrite Rabbit Polyclonal to PAR4 (Cleaved-Gly48) arborization were seen in the two FLP neurons that cover the head region of the worm with a similarly structured mechanosensory arbor, including tangled higher-order branches and loss of characteristic orthogonal dendrites (Figures 1F and 1G). In contrast, a survey of other neuronal classes (branched and unbranched) in showed no major defects in mutants, ruling out a global function in nervous-system patterning for (data not shown). Of note, the commissures of D-type motor neurons, about half of which fasciculate with secondary PVD branches (Smith et al., 2010), seemed to be unaffected in mutants (data not shown). Taken together, the defects in mutants appear to be specific for PVD and FLP dendrites and are not generally observed in other neurons, including those that share the same molecular environment as PVD dendrites. To determine when MNR-1 function is required for PVD dendrite formation, we conducted a series of RNAi experiments starting at different developmental time points. Constitutive knockdown of or or starting merely 12 hr later at the onset of adulthood failed to result in defects in PVD dendrite structure (Figures 1J, S2C, and S2D). These results show a requirement.