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Pbx4 limits vertebrate heart size and promotes pharyngeal arch artery development through partitioning progenitor fates within the second heart field and restricting proliferation

ABSTRACT: Pbx4 limits vertebrate heart size and promotes pharyngeal arch artery development through partitioning progenitor fates within the second heart field and restricting proliferation

PROVIDER: PRJNA522917 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8592250.fastq.gz	Fastqsanger.gz
	SRR8592251.fastq.gz	Fastqsanger.gz
	SRR8592248.fastq.gz	Fastqsanger.gz
	SRR8592249.fastq.gz	Fastqsanger.gz

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Pbx4 limits vertebrate heart size and promotes pharyngeal arch artery development through partitioning progenitor fates within the second heart field and restricting proliferation

Project description:Development of the vertebrate heart requires the appropriate integration of temporally-distinct differentiating progenitor populations. While factors that promote accrual of later-differentiating second heart field (SHF)-derived cells to the outflow tract (OFT) have been intensively investigated, few signals are understood that specifically restrict the size of the vertebrate OFT. Here, we show that improper specification and proliferation of SHF progenitors in zebrafish lazarus (lzr) mutants, which lack the transcription factor Pbx4, produces enlarged hearts with a specific increase in ventricular cardiomyocytes and smooth muscle cells within the OFT. Specifically, optogenetic lineage-tracing demonstrates Pbx4 initially promotes the proper partitioning of the SHF into anterior progenitors, which contribute to the OFT, and adjacent endothelial cell progenitors, which contribute to posterior pharyngeal arch arteries. Subsequently, Pbx4 also limits the size of the SHF through repressing SHF progenitor proliferation. Single-cell RNA sequencing of nkx2.5+ cells revealed that the enlarged SHF progenitor population within Pbx4-deficient embryos assimilates characteristics of normally distinct proliferative and more anterior, differentiated cardiomyocyte populations. Therefore, the generation of proper OFT size and great arteries in vertebrates requires Pbx-dependent stratification of unique progenitor differentiation states to facilitate homeotic-like transformations and limit progenitor production within the SHF.

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Nkx2.5 regulates Jarid2 during outflow tract morphogenesis

Project description:The transcription factor Nkx2.5 is required for specification of pharyngeal arch second heart field (SHF) progenitors that contribute to outflow tract (OFT) and right ventricle (RV) formation. Multiple sets of microarray data were analyzed to identify genes that are candidate targets of Nkx2.5 in the second heart field. These sets are: 1) publicly available data for cardiothoracic tissue from E9.5 Nkx2.5 wild-type, heterozygous and homozygous embryos; 2) an analysis of mouse E10.5 pharyngeal arch tissue; 3) an analysis of mouse E12.5 heart tissue; and 4) a temporal analysis of the cardiogenic cell line P19CL6. This combined analysis identified 11 genes (Lrrn1, Elovl2, Safb, Slc39a6, Khdrbs1, Hoxb4, Fez1, Ccdc117, Jarid2, Nrcam, and Enpp3) expressed in SHF-containing pharyngeal arch tissue whose regulation is dependent on Nkx2.5 expression. Refer to individual Series

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Pbx4 limits heart size and fosters arch artery formation by partitioning second heart field progenitors and restricting proliferation.

Project description:Vertebrate heart development requires the integration of temporally distinct differentiating progenitors. However, few signals are understood that restrict the size of the later-differentiating outflow tract (OFT). We show that improper specification and proliferation of second heart field (SHF) progenitors in zebrafish lazarus (lzr) mutants, which lack the transcription factor Pbx4, produces enlarged hearts owing to an increase in ventricular and smooth muscle cells. Specifically, Pbx4 initially promotes the partitioning of the SHF into anterior progenitors, which contribute to the OFT, and adjacent endothelial cell progenitors, which contribute to posterior pharyngeal arches. Subsequently, Pbx4 limits SHF progenitor (SHFP) proliferation. Single cell RNA sequencing of nkx2.5+ cells revealed previously unappreciated distinct differentiation states and progenitor subpopulations that normally reside within the SHF and arterial pole of the heart. Specifically, the transcriptional profiles of Pbx4-deficient nkx2.5+ SHFPs are less distinct and display characteristics of normally discrete proliferative progenitor and anterior, differentiated cardiomyocyte populations. Therefore, our data indicate that the generation of proper OFT size and arch arteries requires Pbx-dependent stratification of unique differentiation states to facilitate both homeotic-like transformations and limit progenitor production within the SHF.

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