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Transcriptomic insights into fate choice of pallial versus subpallial GABAergic neurons (scRNA-Seq)

ABSTRACT: Transcriptomic insights into fate choice of pallial versus subpallial GABAergic neurons (scRNA-Seq)

PROVIDER: PRJNA1124995 | ENA |

REPOSITORIES: ENA

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Transcriptomic insights into fate choice of pallial versus subpallial GABAergic neurons

Project description:Transcriptomic insights into fate choice of pallial versus subpallial GABAergic neurons

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Transcriptomic insights into fate choice of pallial versus subpallial GABAergic neurons

Project description:The connectivity, activity, and plasticity of the telencephalon are shaped by pallial and subpallial GABAergic neurons, two large populations that are produced in the embryonic medial, caudal and lateral ganglionic eminences in a highly complicated manner. Dysregulated development of GABAergic neurons is associated with neuropsychiatric disorders. However, knowledge about the specification of GABAergic neuron subtypes is limited. Here, using single-cell RNA sequencing combined with loss-of-function we delineated developmental trajectories and revealed transcriptional programs that specify GABAergic neuron subtypes in each GE lineage and transcription factors that direct lineage bifurcation decisions. Our study illuminates the control of production between pallial and subpallial populations and offers transcriptomic insights into the pathogenesis of GABAergic neuron-related disorders.

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Transcriptomic insights into fate choice of pallial versus subpallial GABAergic neurons (CUT&Tag)

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Transcriptomic insights into fate choice of pallial versus subpallial GABAergic neurons (scRNA-Seq)

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Project description:Antigen encounter directs CD4+ T cells to differentiate into T-helper or -regulatory cells. This process focuses the immune response on the invading pathogen and limits tissue damage. Mechanisms that govern -helper versus -regulatory fate remain poorly understood. Here, we show that the E3 ubiquitin ligase Cul5 determines fate selection in CD4+ T cells by regulating IL-4 receptor signaling. Mice lacking Cul5 in T cells developed enhanced Th2 and Th9 inflammation and pathophysiological features of atopic asthma upon allergen exposure. Following T cell activation, Cul5 formed a complex with CIS and pJak1. Loss of Cul5 function resulted in reduced ubiquitylation and increased stability of pJak1, elevated STAT6 activity, and a reduced threshold for IL-4 receptor signaling. In keeping with this, Cul5-deficient T cells deviated from Treg to Th9 differentiation in low IL-4 conditions. These data support that Cul5 promotes a tolerogenic T cell fate choice and reduces susceptibility to allergic asthma.

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Single cell analysis of the postnatal dorsal V-SVZ reveals a role for Bmpr1a-signaling in silencing pallial germinal activity

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