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The researchers mutated a gene that's necessary for new neurons to migrate into the olfactory bulb.
CONCLUSIONS: Preterm birth results in abnormal foveal vascularisation, a failure of the inner retinal neurons to migrate away from the fovea, and an elevated outer nuclear layer ratio.
To test this idea in migrating neurons, we first identified the adhesion receptors used by SVZa neurons to migrate in our ECM substrate.
Lissencephaly results from the failure of vertebrate cortical neurons to migrate properly during development, and is frequently caused by mutations in doublecortin (DCX) [55].
We show that a reelin-dependent ApoER2 downregulation mechanism uncouples newborn neurons from NPCs, thereby enabling neurons to migrate.
These are 'progenitor' cells that develop into the various types of cell found in the cerebellum, and also act as a scaffold for other neurons to migrate across.
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First, we confirmed that planar polarity was normal in the pk1b morphant neuroepithelium and that wild-type FBM neurons could successfully migrate into r6 in a pk1b morphant environment, indicating that the environmental cues to support FBM neuron migration were present even though the host neurons failed to migrate (Fig. 5E,F and Fig. 6D).
Consistent with this, synaptic currents measured in layer 2/3 neurons at PND 8, just after these neurons ceased to migrate, revealed already spatially well-tuned receptive fields.
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).
As neurons continue to migrate well into postnatal stages, we addressed the final positions of neurons generated from all Tbr2+ IPCs in Ai9 brains at postnatal Day 21 (P21, N = 4 animals) after the completion of neuronal migration (Fig. 2 A).
We reasoned that if nhsl1b, vangl2 or scrib mutant FBM neurons fail to migrate in pk1b-depleted hosts, this would mean that the rescue of their migration that we observed in a wild-type environment was mediated by the host FBM neurons themselves.
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