ArticleProceedings of the National Academy of Sciences of the United States of America2012
Knockout of the prion protein (PrP)-like Sprn gene does not produce embryonic lethality in combination with PrP(C)-deficiency.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 65 citations in OpenAlex.
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- Enhanced RNA-targeting CRISPR-Cas technology in zebrafish.Nature communications · 2025Article
- Enhanced RNA-targeting CRISPR-Cas technology in zebrafish.bioRxiv : the preprint server for biology · 2024Article
- Malat1 affects transcription and splicing through distinct pathways in mouse embryonic stem cells.NAR genomics and bioinformatics · 2024Article
- The First Genetic Characterization of theAnimals : an open access journal from MDPI · 2024Article
- TSP50 Attenuates DSS-Induced Colitis by Regulating TGF-β Signaling Mediated Maintenance of Intestinal Mucosal Barrier Integrity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Rethinking the Architecture of Attachment: New Insights into the Role for Oxytocin Signaling.Affective science · 2022Review
- Potential genetic robustness of Prnp and Sprn double knockout mouse embryos towards ShRNA-lentiviral inoculation.Veterinary research · 2022Article
- Membrane Domain Localization and Interaction of the Prion-Family Proteins, Prion and Shadoo with Calnexin.Membranes · 2021Article
- Article
- Genotype to Phenotype: CRISPR Gene Editing Reveals Genetic Compensation as a Mechanism for Phenotypic Disjunction of Morphants and Mutants.International journal of molecular sciences · 2021Review
- Diverse, evolving conformer populations drive distinct phenotypes in frontotemporal lobar degeneration caused by the same MAPT-P301L mutation.Acta neuropathologica · 2020Article
- Proteasomal Inhibition Redirects the PrP-Like Shadoo Protein to the Nucleus.Molecular neurobiology · 2019Article
- Rapid Evolution of Gained Essential Developmental Functions of a Young Gene via Interactions with Other Essential Genes.Molecular biology and evolution · 2019Article
- CRISPR/Cas9-targeted mutagenesis of Os8N3 in rice to confer resistance to Xanthomonas oryzae pv. oryzae.Rice (New York, N.Y.) · 2019Article
- CRISPR-Cas: a tool for cancer research and therapeutics.Nature reviews. Clinical oncology · 2019Review
- Zebrafish as an Emerging Model for Osteoporosis: A Primary Testing Platform for Screening New Osteo-Active Compounds.Frontiers in endocrinology · 2019Review
- Inhibition of cell fate repressors secures the differentiation of the touch receptor neurons ofDevelopment (Cambridge, England) · 2018Article
- Prion gene paralogs are dispensable for early zebrafish development and have nonadditive roles in seizure susceptibility.The Journal of biological chemistry · 2018Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
The Sprn gene encodes Shadoo (Sho), a glycoprotein with biochemical properties similar to the unstructured region of cellular prion protein (PrP(C)). Sho has been considered a candidate for the hypothetical π protein that supplies a PrP(C)-like function to maintain the viability of Prnp(0/0) mice lacking the PrP(C) protein. To understand these relationships more clearly we probed the cell biology of Sho and created knockout mice. Besides full-length and a "C1" C-terminal fragment, we describe a 6-kDa N-terminal Sho neuropeptide, "N1," which is present in membrane-enriched subcellular fractions of wild-type mice. Sprn null alleles were produced that delete all protein coding sequences yet spare the Mtg1 gene transcription unit that overlaps the Sprn 3' UTR; the resulting mice bred to homozygosity were viable and fertile, although Sprn(0/0) mice maintained in two genetic backgrounds weighed less than wild-type mice. Lack of Sho protein did not affect prion incubation time. Contrasting with lethality reported for knockdown of expression in Prnp(0/0) embryos using lentiviruses targeted against the Sprn 3' UTR, we established that double-knockout mice deficient in both Sho and PrP(C) are fertile and viable up to 690 d of age. Our data reduce the impetus for equating Sho with the notional π protein and are not readily reconciled with hypotheses wherein expression of PrP(C) and Sho are both required for completion of embryogenesis. Alternatively, and in accord with some reports for PrP(C), we infer that Sho's activity will prove germane to the maintenance of neuronal viability in postnatal life.
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