Zbtb16 determines the fate plasticity of cardiovascular progenitors through IGF2BP3-mediated mRNA stabilization [scRNA-seq]
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PROVIDER: PRJNA1174780 | ENA |
REPOSITORIES: ENA
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Project description:Cardiovascular progenitors (CPs) are responsible for generating the diverse cell populations in hearts, exhibiting significant transcriptional heterogeneity. However, the regulation of fate plasticity among heterogeneous CP subpopulations, as well as the intrinsic regulatory factors, remains poorly understood. In this study, we characterized three CP subpopulations derived from pluripotent stem cells and found that the deletion of ZBTB family protein Zbtb16 led to a profound imbalance in the branching transition trajectory of Early-CPs, redirecting them toward CPs committed to endothelial cells and cardiac fibroblasts (EC/CF-CPs) rather than that to cardiomyocytes (CM-CPs). Mechanistic studies revealed that Zbtb16 interacted with the m6A reader IGF2BP3 to post-transcriptionally recognize and stabilize the mRNAs of key genes critical for the CM-CP subpopulation determination. Collectively, our findings established Zbtb16 as a key regulator of fate plasticity of heterogeneous CP subpopulations and revealed the interplay with IGF2BP3 to impact the m6A-modified mRNA stabilization, which provided new insights into the intrinsic connections between CP subpopulation plasticity and cardiovascular multi-lineage fate determination.
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Project description:Cardiovascular progenitors (CPs) are responsible for generating the diverse cell populations in hearts, exhibiting significant transcriptional heterogeneity. However, the regulation of fate plasticity among heterogeneous CP subpopulations, as well as the intrinsic regulatory factors, remains poorly understood. In this study, we characterized three CP subpopulations derived from pluripotent stem cells and found that the deletion of ZBTB family protein Zbtb16 led to a profound imbalance in the branching transition trajectory of Early-CPs, redirecting them toward CPs committed to endothelial cells and cardiac fibroblasts (EC/CF-CPs) rather than that to cardiomyocytes (CM-CPs). Mechanistic studies revealed that Zbtb16 interacted with the m6A reader IGF2BP3 to post-transcriptionally recognize and stabilize the mRNAs of key genes critical for the CM-CP subpopulation determination. Collectively, our findings established Zbtb16 as a key regulator of fate plasticity of heterogeneous CP subpopulations and revealed the interplay with IGF2BP3 to impact the m6A-modified mRNA stabilization, which provided new insights into the intrinsic connections between CP subpopulation plasticity and cardiovascular multi-lineage fate determination.
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Project description:Zbtb16 determines the fate plasticity of cardiovascular progenitors through IGF2BP3-mediated mRNA stabilization [RIP-Seq]
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Project description:Recent genomic studies suggest that a single gene is involved in multiple diseases, however it is unclear what mechanism destined for different diseases by a single gene. Mutations of ZBTB16 are associated with autism spectrum disorder (ASD) and schizophrenia (SCZ), but how ZBTB16 fates ASD or SCZ are unknown. Here we show the deletion of Zbtb16 in mice leads to both ASD- and SCZ-like behaviors such as social impairment, repetitive behaviors, risk-taking behaviors, and cognitive impairment. To elucidate the mechanism underlying the behavioral phenotypes, we carried out histological studies and observed impairments in thinning of neocortical layer 6 (L6) and a reduction of TBR1+ neurons in the prefrontal cortex (PFC) of Zbtb16 KO mice. Furthermore, we found increased dendritic spines and microglia as well as developmental defects in oligodendrocytes and neocortical myelination in the PFC of Zbtb16 KO mice. Using a genomics approach, we identified the Zbtb16-transcriptome that includes genes involved in both ASD and SCZ pathophysiology and neocortical maturation such as neurogenesis and myelination. Co-expression networks further identified Zbtb16-correlated modules that are unique to ASD or SCZ respectively. Our study provides insight into the differential role of the single gene ZBTB16 in ASD and SCZ.
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