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Heterogeneous fates of simultaneously-born neurons in the cortical ventricular zone

ABSTRACT: Heterogeneous fates of simultaneously-born neurons in the cortical ventricular zone

PROVIDER: PRJNA790452 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17269327.fastq.gz	Fastqsanger.gz
	SRR17269328.fastq.gz	Fastqsanger.gz
	SRR17269329.fastq.gz	Fastqsanger.gz
	SRR17269330.fastq.gz	Fastqsanger.gz
	SRR17269333.fastq.gz	Fastqsanger.gz

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Heterogeneous fates of simultaneously-born neurons in the cortical ventricular zone

Project description:Neocortical excitatory neurons belong to diverse cell types, which can be distinguished by their dates of birth, laminar location, connectivity and molecular identities. During embryogenesis, apical progenitors (APs) located in the ventricular zone first give birth to deep-layer neurons, and next to superficial-layer neurons. While the overall sequential construction of neocortical layers is well-established, whether multiple neuron types are produced by APs at single time points of corticogenesis is unknown. To address this question, here we used FlashTag to fate-map simultaneously-born (i.e. isochronic) cohorts of AP-born neurons at successive stages of corticogenesis. We reveal that early in corticogenesis, isochronic neurons differentiate into heterogeneous laminar, hodological and molecular cell types. Later on, instead, simultaneously-born neurons have more homogeneous fates. Using single-cell gene expression analyses, we identify an early postmitotic surge in the molecular heterogeneity of nascent neurons during which some early-born neurons initiate and partially execute late-born neuron transcriptional programs. Together, these findings suggest that as corticogenesis unfolds, mechanisms allowing increased homogeneity in neuronal output are progressively implemented, resulting in progressively more predictable neuronal identities.

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Heterogeneous fates of simultaneously-born neurons during early corticogenesis

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Heterogeneous fates of simultaneously-born neurons during early corticogenesis

Project description:We labelled isochronic cohorts of mouse cortical neurons and analyzed their contribution to the diversity of cortical neurons. We find that early born neurons contribute to a large diversity of cortical neuron subtypes, asa also confirmed by the transcsriptomic analysis of E13.5 born neurons through Patchseq. Ultimately we identify eaarly differentiation of early born neurons as the instance characterized by the highest tranascriptomical variability which intermingles deep layer identity genes with upper layer specific ones.

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Heterogeneous fates of simultaneously-born neurons in the cortical ventricular zone.

Project description:Neocortical excitatory neurons belong to diverse cell types, which can be distinguished by their dates of birth, laminar location, connectivity, and molecular identities. During embryogenesis, apical progenitors (APs) located in the ventricular zone first give birth to deep-layer neurons, and next to superficial-layer neurons. While the overall sequential construction of neocortical layers is well-established, whether APs produce multiple neuron types at single time points of corticogenesis is unknown. To address this question, here we used FlashTag to fate-map simultaneously-born (i.e. isochronic) cohorts of AP daughter neurons at successive stages of corticogenesis. We reveal that early in corticogenesis, isochronic neurons differentiate into heterogeneous laminar, hodological and molecular cell types. Later on, instead, simultaneously-born neurons have more homogeneous fates. Using single-cell gene expression analyses, we identify an early postmitotic surge in the molecular heterogeneity of nascent neurons during which some early-born neurons initiate and partially execute late-born neuron transcriptional programs. Together, these findings suggest that as corticogenesis unfolds, mechanisms allowing increased homogeneity in neuronal output are progressively implemented, resulting in progressively more predictable neuronal identities.

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PRDM16 is required for proper specification of the working ventricular myocardium by suppressing alternative cardiomyocyte cell fates.

Project description:PRDM16 is a transcription factor with histone methyltransferase activity expressed at the earliest stages of cardiac development. Pathogenic mutations in humans lead to cardiomyopathy, conduction abnormalities and heart failure. PRDM16 is specifically expressed in ventricular but not atrial cardiomyocytes and declines in expression postnatally. Since in other tissues PRDM16 is best known for its role in binary cell fate decisions, we hypothesized a similar decision-making function in cardiomyocytes. Here, we demonstrated that cardiomyocyte-specific deletion of Prdm16 during cardiac development results in contractile dysfunction and abnormal electrophysiology of the postnatal heart, resulting in premature death. By combined RNA+ATAC single-cell sequencing we found that PRDM16 favors ventricular working cardiomyocyte identity, by opposing the activity of master regulators of atrial and ventricular conduction fate. Myocardial loss of Prdm16 during development resulted in hyperplasia of the ventricular conduction system. Hence, PRDM16 plays an indispensable role during cardiac development by driving ventricular working cardiomyocyte identity.

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PRDM16 is required for proper specification of the working ventricular myocardium by suppressing alternative cardiomyocyte cell fates.

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Adult ventricular cardiomyocytes

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