ArticlePloS one2009
Analysis of blood stem cell activity and cystatin gene expression in a mouse model presenting a chromosomal deletion encompassing Csta and Stfa2l1.
Article in PloS one, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 16 citations in OpenAlex.
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- Inducible disruption ofProceedings of the National Academy of Sciences of the United States of America · 2023Article
- The intermembrane space protein Mix23 is a novel stress-induced mitochondrial import factor.The Journal of biological chemistry · 2020Article
- Site-1 protease ablation in the osterix-lineage in mice results in bone marrow neutrophilia and hematopoietic stem cell alterations.Biology open · 2020Article
- Bioinformatics Analyses Determined the Distinct CNS and Peripheral Surrogate Biomarker Candidates Between Two Mouse Models for Progressive Multiple Sclerosis.Frontiers in immunology · 2019Article
- Expression profiling of genes regulated by sphingosine kinase1 signaling in a murine model of hyperoxia induced neonatal bronchopulmonary dysplasia.BMC genomics · 2017Article
- Article
- Identification and characterization of long intergenic non-coding RNAs related to mouse liver development.Molecular genetics and genomics : MGG · 2014Article
- Article
- Mutations in CSTA, encoding Cystatin A, underlie exfoliative ichthyosis and reveal a role for this protease inhibitor in cell-cell adhesion.American journal of human genetics · 2011Article
- Modulation of cystatin A expression in human airway epithelium related to genotype, smoking, COPD, and lung cancer.Cancer research · 2011Article
- Genome-wide interrogation of Mammalian stem cell fate determinants by nested chromosome deletions.PLoS genetics · 2010Article
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
The cystatin protein superfamily is characterized by the presence of conserved sequences that display cysteine protease inhibitory activity (e.g., towards cathepsins). Type 1 and 2 cystatins are encoded by 25 genes of which 23 are grouped in 2 clusters localized on mouse chromosomes 16 and 2. The expression and essential roles of most of these genes in mouse development and hematopoiesis remain poorly characterized. In this study, we describe a set of quantitative real-time PCR assays and a global expression profile of cystatin genes in normal mouse tissues. Benefiting from our collection of DelES embryonic stem cell clones harboring large chromosomal deletions (to be reported elsewhere), we selected a clone in which a 95-kb region of chromosome 16 is missing (Del(16qB3Delta/+)). In this particular clone, 2 cystatin genes, namely Csta and Stfa2l1 are absent along with 2 other genes (Fam162a, Ccdc58) and associated intergenic regions. From this line, we established a new homozygous mutant mouse model (Del(16qB3Delta/16qB3Delta)) to assess the in vivo biological functions of the 2 deleted cystatins. Stfa2l1 gene expression is high in wild-type fetal liver, bone marrow, and spleen, while Csta is ubiquitously expressed. Homozygous Del(16qB3Delta/16qB3Delta) animals are phenotypically normal, fertile, and not overtly susceptible to spontaneous or irradiation-induced tumor formation. The hematopoietic stem and progenitor cell activity in these mutant mice are also normal. Interestingly, quantitative real-time PCR expression profiling reveals a marked increase in the expression levels of Stfa2l1/Csta phylogenetically-related genes (Stfa1, Stfa2, and Stfa3) in Del(16qB3Delta/16qB3Delta) hematopoietic tissues, suggesting that these candidate genes might be contributing to compensatory mechanisms. Overall, this study presents an optimized approach to globally monitor cystatin gene expression as well as a new mouse model deficient in Stfa2l1/Csta genes, expanding the available tools to dissect cystatin roles under normal and pathological conditions.
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