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In FBM neuron migration, previous chimeric analyses have suggested that the PCP components Vangl2, Fzd3a and Celsr2 act primarily non cell-autonomously, as wild-type neurons fail to migrate through a mutant neuroepithelium and mutant neurons do migrate through a wild-type environment, albeit incompletely (Jessen et al., 2002; Wada et al., 2005; Wada et al., 2006).
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Consequently the loss of synaptic vesicle release in mutant neurons does not affect neurite outgrowth enough to prevent the formation of long-distance projections.
Other aspects of overall MB neuron morphology seemed normal in the mutant, and the presence of a small number of mutant neurons did not affect the lifespan of the animals (supplementary material Fig. S6).
Despite the severe patterning and field coverage defects, Ret mutant C4da neurons did not show a significant reduction in total dendrite length.
Moreover, this Cut-HA expression in Cp1-mutant ddaC neurons did not recover dendrite regrowth defects.
This suggests that ARC anorexigenic neurons are generated in Nkx2.1iCre/+ Ngn3 flox/flox mutants, albeit that a subset of these neurons do not express Pomc and Pdyn.
Visualization of GFP-labeled DA neurons on the mutant backgrounds verified that gross morphologic deficits of DA neurons do not account for the Swip phenotype of the lines presented in the current report.
Restoration of CRH-1 in AFD of CREB-depleted crh-1 mutants rescues its thermotactic defect, whereas restorations in other neurons do not.
DOI: http://dx.doi.org/10.7554/eLife.05491.003 10.7554/eLiFigure91 figuregure 1—figure supplement 1. Class I da neurons do not display obvious morphological defects in Ret mutant animals.
Archetypal neurons don't compute this way.
Finally, A11 neurons do not express DAT.
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