FOXG1 drives transcriptomic networks to specify principal neuron subtypes during the development of the medial pallium

Author:

Ba Ru1ORCID,Yang Lin2ORCID,Zhang Baoshen1ORCID,Jiang Pengfei1ORCID,Ding Zhipeng1ORCID,Zhou Xue1ORCID,Yang Zhengang2ORCID,Zhao Chunjie1ORCID

Affiliation:

1. Key Laboratory of Developmental Genes and Human Diseases, Ministry of Education, School of Medicine, Southeast University, Nanjing 210009, China.

2. State Key Laboratory of Medical Neurobiology, Institutes of Brain Science, MOE Frontier Research Center for Brain Science, Fudan University, Shanghai 200032, P.R. China.

Abstract

The medial pallium (MP) is the major forebrain region underlying learning and memory, spatial navigation, and emotion; however, the mechanisms underlying the specification of its principal neuron subtypes remain largely unexplored. Here, by postmitotic deletion of FOXG1 (a transcription factor linked to autism spectrum disorders and FOXG1 syndrome) and single-cell RNA sequencing of E17.5 MP in mice, we found that FOXG1 controls the specification of upper-layer retrosplenial cortical pyramidal neurons [RSC-PyNs (UL)], subiculum PyNs (SubC-PyNs), CA1-PyNs, CA3-PyNs, and dentate gyrus granule cells (DG-GCs) in the MP. We uncovered subtype-specific and subtype-shared FOXG1-regulated transcriptomic networks orchestrating MP neuron specification. We further demonstrated that FOXG1 transcriptionally represses Zbtb20 , Prox1 , and Epha4 to prevent CA3-PyN and DG-GC identities during the specification of RSC-PyNs (UL) and SubC-PyNs; FOXG1 directly activates Nr4a2 to promote SubC-PyN identity. We showed that TBR1, controlled by FOXG1 during CA1-PyN specification, was down-regulated. Thus, our study illuminates MP principal neuron subtype specification and related neuropathogenesis.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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