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Gene Review

Snrpn  -  small nuclear ribonucleoprotein N

Mus musculus

Synonyms: 2410045I01Rik, HCERN3, Peg4, Pwcr1, SMN, ...
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Disease relevance of Snrpn


High impact information on Snrpn

  • We show here that a 0.9-kb deletion of exon 1 of mouse Snrpn did not disrupt imprinting or elicit any obvious phenotype, although it did allow the detection of previously unknown upstream exons [6].
  • Here we show that a minitransgene composed of a 200-bp Snrpn promoter/exon1 and a 1-kb sequence located approximately 35 kb upstream to the SNRPN promoter confer imprinting as judged by differential methylation, parent-of-origin-specific transcription and asynchronous replication [7].
  • Deletion of the SNRPN promoter/exon 1 region (the PWS IC element) appears to impair the establishment of the paternal imprint in the male germ line and leads to PWS [8].
  • A related control element was isolated in the mouse Snrpn genomic region which, when deleted on the paternally inherited chromosome, resulted in the loss of expression of all four genes and early post-natal lethality [9].
  • Gene expression studies established that Snrpn is not expressed in mice with the maternal duplication and suggest that the closely-linked Gabrb-3 locus is not subject to imprinting [2].

Biological context of Snrpn

  • In this in vivo study, histone methylation and acetylation are investigated along the imprinted mouse genes Snrpn, Igf2r and U2af1-rs1 [10].
  • We examined the methylation status of Snrpn during oocyte growth and maturation [11].
  • Moreover, using mice with only maternal copies of Snrpn (maternal duplication for the chromosome region involved and parthenogenotes), we have shown that the gene is imprinted in all of these tissues and, generally, from the time the gene is first expressed at 7.5 days gestation [12].
  • Hence, we set out to investigate the epigenetic stability of neuronal genes and analyzed DNA methylation patterns in the Snurf/Snrpn imprinted cluster in several cultured mouse ES cell lines [13].
  • Maternal and paternal genomes function independently in mouse ova in establishing expression of the imprinted genes Snrpn and Igf2r: no evidence for allelic trans-sensing and counting mechanisms [14].

Anatomical context of Snrpn


Associations of Snrpn with chemical compounds

  • For H4, underacetylation of the maternal allele was exclusively (U2af1-rs1) or predominantly (Snrpn) at lysine 5 [17].
  • At Snrpn, no changes in acetylation were observed in the TSA-treated cells [18].
  • Bisulfite sequencing revealed that reactivation of maternal alleles of Peg3 and Snrpn in specific tissues was accompanied by partial demethylation at their potential imprinting control regions [19].

Other interactions of Snrpn

  • The Igf2r and Snrpn genes were activated by the early 4-cell stage and exhibited biallelic and monoallelic expression, respectively, throughout preimplantation development [15].
  • Although Snrpn, Ipw and MBII-85 are putatively transcribed from the same promoter, the transcripts are differentially detected in neural tissues [20].
  • On the other hand, the Zfp127/Snrpn locus showed such an allele-specific fractionation pattern only in F(1) hybrid mice of a cross but not in those of the reciprocal cross [21].
  • To examine this possibility, we introduced sequences from the DMDs of the imprinted Igf2r, H19, and Snrpn genes into a nonimprinted derivative of the normally imprinted RSVIgmyc transgene, created by excising its own DMD [22].
  • We show by RNA fluorescence in situ hybridization (FISH) that expression of Snrpn, an imprinted gene regulated by the PWS-IC, is biallelic in G9a -/- ES cells, indicating loss of imprinting [23].

Analytical, diagnostic and therapeutic context of Snrpn


  1. Paternal deletion from Snrpn to Ube3a in the mouse causes hypotonia, growth retardation and partial lethality and provides evidence for a gene contributing to Prader-Willi syndrome. Tsai, T.F., Jiang, Y.H., Bressler, J., Armstrong, D., Beaudet, A.L. Hum. Mol. Genet. (1999) [Pubmed]
  2. A candidate mouse model for Prader-Willi syndrome which shows an absence of Snrpn expression. Cattanach, B.M., Barr, J.A., Evans, E.P., Burtenshaw, M., Beechey, C.V., Leff, S.E., Brannan, C.I., Copeland, N.G., Jenkins, N.A., Jones, J. Nat. Genet. (1992) [Pubmed]
  3. Characterization of the human Snrpn minimal promoter and cis elements within it. Green Finberg, Y., Kantor, B., Hershko, A.Y., Razin, A. Gene (2003) [Pubmed]
  4. Cloning and sequencing of a mouse embryonal carcinoma cell mRNA encoding the tissue specific RNA splicing protein SmN. Gerrelli, D., Sharpe, N.G., Latchman, D.S. Nucleic Acids Res. (1991) [Pubmed]
  5. Immunogenic properties of synthetic fragments of Sm-D protein in normal and lupus mice. Winska-Wiloch, H., Muller, S., Katz, D.R., Wilkinson, L., Hutchings, P.R., Isenberg, D.A. Lupus (1997) [Pubmed]
  6. The SNRPN promoter is not required for genomic imprinting of the Prader-Willi/Angelman domain in mice. Bressler, J., Tsai, T.F., Wu, M.Y., Tsai, S.F., Ramirez, M.A., Armstrong, D., Beaudet, A.L. Nat. Genet. (2001) [Pubmed]
  7. The imprinting box of the Prader-Willi/Angelman syndrome domain. Shemer, R., Hershko, A.Y., Perk, J., Mostoslavsky, R., Tsuberi, B., Cedar, H., Buiting, K., Razin, A. Nat. Genet. (2000) [Pubmed]
  8. De novo deletions of SNRPN exon 1 in early human and mouse embryos result in a paternal to maternal imprint switch. Bielinska, B., Blaydes, S.M., Buiting, K., Yang, T., Krajewska-Walasek, M., Horsthemke, B., Brannan, C.I. Nat. Genet. (2000) [Pubmed]
  9. Disruption of the mouse necdin gene results in early post-natal lethality. Gérard, M., Hernandez, L., Wevrick, R., Stewart, C.L. Nat. Genet. (1999) [Pubmed]
  10. Allele-specific histone lysine methylation marks regulatory regions at imprinted mouse genes. Fournier, C., Goto, Y., Ballestar, E., Delaval, K., Hever, A.M., Esteller, M., Feil, R. EMBO J. (2002) [Pubmed]
  11. Methylation dynamics of imprinted genes in mouse germ cells. Lucifero, D., Mertineit, C., Clarke, H.J., Bestor, T.H., Trasler, J.M. Genomics (2002) [Pubmed]
  12. Ubiquitous expression and imprinting of Snrpn in the mouse. Barr, J.A., Jones, J., Glenister, P.H., Cattanach, B.M. Mamm. Genome (1995) [Pubmed]
  13. Influence of in vitro manipulation on the stability of methylation patterns in the Snurf/Snrpn-imprinting region in mouse embryonic stem cells. Schumacher, A., Doerfler, W. Nucleic Acids Res. (2004) [Pubmed]
  14. Maternal and paternal genomes function independently in mouse ova in establishing expression of the imprinted genes Snrpn and Igf2r: no evidence for allelic trans-sensing and counting mechanisms. Szabó, P.E., Mann, J.R. EMBO J. (1996) [Pubmed]
  15. Allele-specific expression and total expression levels of imprinted genes during early mouse development: implications for imprinting mechanisms. Szabó, P.E., Mann, J.R. Genes Dev. (1995) [Pubmed]
  16. Structure of the imprinted mouse Snrpn gene and establishment of its parental-specific methylation pattern. Shemer, R., Birger, Y., Riggs, A.D., Razin, A. Proc. Natl. Acad. Sci. U.S.A. (1997) [Pubmed]
  17. DNA methylation is linked to deacetylation of histone H3, but not H4, on the imprinted genes Snrpn and U2af1-rs1. Gregory, R.I., Randall, T.E., Johnson, C.A., Khosla, S., Hatada, I., O'Neill, L.P., Turner, B.M., Feil, R. Mol. Cell. Biol. (2001) [Pubmed]
  18. Inhibition of histone deacetylases alters allelic chromatin conformation at the imprinted U2af1-rs1 locus in mouse embryonic stem cells. Gregory, R.I., O'Neill, L.P., Randall, T.E., Fournier, C., Khosla, S., Turner, B.M., Feil, R. J. Biol. Chem. (2002) [Pubmed]
  19. Widespread disruption of genomic imprinting in adult interspecies mouse (Mus) hybrids. Shi, W., Krella, A., Orth, A., Yu, Y., Fundele, R. Genesis (2005) [Pubmed]
  20. Prader-Willi syndrome transcripts are expressed in phenotypically significant regions of the developing mouse brain. Lee, S., Walker, C.L., Wevrick, R. Gene Expr. Patterns (2003) [Pubmed]
  21. Differential chromatin packaging of genomic imprinted regions between expressed and non-expressed alleles. Watanabe, T., Yoshimura, A., Mishima, Y., Endo, Y., Shiroishi, T., Koide, T., Sasaki, H., Asakura, H., Kominami, R. Hum. Mol. Genet. (2000) [Pubmed]
  22. Shared role for differentially methylated domains of imprinted genes. Reinhart, B., Eljanne, M., Chaillet, J.R. Mol. Cell. Biol. (2002) [Pubmed]
  23. Role of histone methyltransferase G9a in CpG methylation of the Prader-Willi syndrome imprinting center. Xin, Z., Tachibana, M., Guggiari, M., Heard, E., Shinkai, Y., Wagstaff, J. J. Biol. Chem. (2003) [Pubmed]
  24. Evidence for translational regulation of the imprinted Snurf-Snrpn locus in mice. Tsai, T.F., Chen, K.S., Weber, J.S., Justice, M.J., Beaudet, A.L. Hum. Mol. Genet. (2002) [Pubmed]
  25. The intronless mouse gene for the tissue specific splicing protein SmN is a processed pseudogene containing a stop codon after thirty-one amino acids. Grimaldi, K., Gerrelli, D., Sharpe, N.G., Lund, T., Latchman, D.S. DNA Seq. (1992) [Pubmed]
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