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Mouse models of neutropenia reveal progenitor-stage-specific defects [CITE-Seq]

ABSTRACT: Mouse models of neutropenia reveal progenitor-stage-specific defects [CITE-Seq]

PROVIDER: PRJNA596675 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10741177.fastq.gz	Fastqsanger.gz
	SRR10741178.fastq.gz	Fastqsanger.gz
	SRR10741179.fastq.gz	Fastqsanger.gz
	SRR10741180.fastq.gz	Fastqsanger.gz
	SRR10741181.fastq.gz	Fastqsanger.gz

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Mouse models of neutropenia reveal progenitor-stage-specific defects [CITE-Seq]

Project description:Advances in genetics and sequencing have lead to a deluge of disease-associated and disease-causing genetic alterations. Resolving causality between genetics and disease requires generating accurate models for molecular dissection; however, the rapid expansion of single-cell landscapes presents a major challenge to accurate comparisons between mutants and their wild type equivalents. Here, we generated mouse models of human severe congenital neutropenia (SCN) using patient-derived mutations in the Growth factor independent-1 (GFI1) transcription factor. To delineate the impact of SCN mutations, we first generated single-cell references for granulopoietic genomic states with linked epitopes, then developed a new computational approach to align mutant cells to their wild-type equivalent and derive differentially expressed genes. Surprisingly, the majority of differentially expressed GFI1-target genes are sequentially altered as cells traverse successive states. These cell-state-specific insights facilitated genetic rescue of granulocytic specification but not post-commitment defects in the expression of innate-immune effectors, providing regulatory insights into granulocyte dysfunction.

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Project description:Advances in genetics and sequencing have identified a plethora of disease-associated and disease-causing genetic alterations. To determine causality between genetics and disease, accurate models for molecular dissection are required; however, the rapid expansion of transcriptional populations identified through single-cell analyses presents a major challenge for accurate comparisons between mutant and wild-type cells. Here we generate mouse models of human severe congenital neutropenia (SCN) using patient-derived mutations in the GFI1 transcription factor. To determine the effects of SCN mutations, we generated single-cell references for granulopoietic genomic states with linked epitopes1, aligned mutant cells to their wild-type equivalents and identified differentially expressed genes and epigenetic loci. We find that GFI1-target genes are altered sequentially, as cells go through successive states of differentiation. These insights facilitated the genetic rescue of granulocytic specification but not post-commitment defects in innate immune effector function, and underscore the importance of evaluating the effects of mutations and therapy within each relevant cell state.

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