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Gene Review

Rnaseh1  -  ribonuclease H1

Mus musculus

Synonyms: RNase H1, Ribonuclease H1, Rnh1
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Disease relevance of Rnaseh1

  • Sequence alignments indicate that MLV Y586 is equivalent to HIV-1 Y501, a component of the recently described RNase H primer grip domain, which contacts and positions the DNA primer strand near the RNase H active site [1].
  • As compared to the attenuated virus from cultures of 5-86 and G-2 cells, the subunits of the RNA from the virions of SQ-A cells are the same size, and the amount of reverse transcriptase activity and RNase H present in the purified virions of the three lines are similar [2].
  • The reverse transcriptase enzymes of retroviruses are multifunctional proteins containing both DNA polymerase activity and a nuclease activity, termed RNase H, specific for RNA in RNA-DNA hybrid form [3].
  • Escherichia coli RNase H has a basic extension that is involved in binding nucleic acid substrates [4].
  • This basic extension is present in the RNase H of Moloney murine leukemia virus reverse transcriptase (MLV RT), but has been deleted from the RNase H of HIV-1 RT [4].

High impact information on Rnaseh1

  • As expected, oligo-nucleotide-directed RNase H cleavage of this portion of murine U7 inhibits the in vitro processing reaction [5].
  • These findings indicate that the RNase H primer grip can affect the template-primer conformation at the polymerase active site and that the MLV Y586 residue and template-primer conformation are important determinants of RT fidelity [1].
  • The relative contributions of polymerase-dependent and polymerase-independent RNase H activities during reverse transcription and template switching in vivo have not been determined [6].
  • Dynamic copy choice: steady state between murine leukemia virus polymerase and polymerase-dependent RNase H activity determines frequency of in vivo template switching [6].
  • Because only polymerase-independent RNase H activity is present in this cell line, the relative roles of polymerase-dependent and -independent RNase H activities in template switching could be determined [6].

Biological context of Rnaseh1


Anatomical context of Rnaseh1

  • Freshly prepared reticulocyte lysates were found to contain 1-2% of the level of RNase H in nucleated cells [10].
  • The relative roles of these three types of Na+/Pi co-transporters in Pi transport in mouse kidney cortex have now been investigated by RNase H-mediated hybrid depletion [11].
  • When poly(A) tracts were selectively removed from germ cell RNAs by ribonuclease H treatment, identical 1.3-kb CD-MPR mRNAs were detected in pachytene spermatocytes and round spermatids, indicating that the size difference between the 1.4- and 1.6-kb transcripts is due to variations in poly(A) tail length.(ABSTRACT TRUNCATED AT 250 WORDS)[12]
  • Using the mFold program, we designed seven anti-pCD ribozymes and checked the accessibility to target pCD mRNA by RNase H cleavage experiment in a cell-free system [13].
  • Hybridized RNA is then detected by incubation of membranes with Escherichia coli RNase H and DNA polymerase I. RNase H is used for nicking the RNA in the hybrids [14].

Associations of Rnaseh1 with chemical compounds

  • Additionally, trans-complementation of RNase H mutants in the presence and absence of hydroxyurea, which slows the rate of reverse transcription, showed that hydroxyurea increased template switching only when polymerase-dependent RNase H activity was present [6].
  • Thus an RNase H-dependent phosphorothioate oligodeoxynucleotide can be modified as a 2'-O-propyl 'chimeric' oligonucleotide to provide a significant increase in antisense activity in cell culture [15].
  • The resulting RNase H-mediated cleavages in the cell extracts were quantified using RT-PCR with fluorescein and rhodaminetagged primers to generate fluorescent products that are analyzed and quantified on an automated DNA sequencer [16].
  • Differential inhibition of DNA polymerase and RNase H activities of the reverse transcriptase by phosphonoformate [17].
  • Only antisense ONs acting via an RNase H mechanism or by steric hindrance through covalent attachment (via transplatin modification) to the target mRNA were found to definitively arrest translation in this study [9].

Enzymatic interactions of Rnaseh1

  • An ODN binding site in native MTase mRNA was identified that was cleaved by endogenous RNase H with an efficiency of 85% in the extracts [16].

Regulatory relationships of Rnaseh1

  • Ribonuclease H analysis revealed that this T3-induced decrease in size was due to a shortening of poly(A) tail from approximately 160 to approximately 30 nucleotides and was specific for TSHbeta mRNA [18].

Other interactions of Rnaseh1

  • RNase H analysis showed that the size difference between the two testicular Hoxa-4 transcripts of 1.35 and 1.45 kb was due to a postmeiotic increase in poly(A) tail length [19].
  • The presence of RNase A, but not RNase H, inhibited exonucleolytic digestion, suggesting that a ribonucleoprotein is responsible for the exonucleolysis [20].
  • The 16S RNA was annealed to globin cDNA and the hybrid digested with ribonuclease H. The undigested fragment did not bind to oligo(dT)-cellulose and its size was that expected for the intact 5' portion of the precursor [21].

Analytical, diagnostic and therapeutic context of Rnaseh1


  1. Y586F mutation in murine leukemia virus reverse transcriptase decreases fidelity of DNA synthesis in regions associated with adenine-thymine tracts. Zhang, W.H., Svarovskaia, E.S., Barr, R., Pathak, V.K. Proc. Natl. Acad. Sci. U.S.A. (2002) [Pubmed]
  2. Characterization of leukemogenic virus produced by a new line of Friend erythroleukemia virus-transformed cells. Friend, C., Pogo, B.G., Holland, J.G. Proc. Natl. Acad. Sci. U.S.A. (1984) [Pubmed]
  3. Abortive reverse transcription by mutants of Moloney murine leukemia virus deficient in the reverse transcriptase-associated RNase H function. Tanese, N., Telesnitsky, A., Goff, S.P. J. Virol. (1991) [Pubmed]
  4. The basic loop of the RNase H domain of MLV RT is important both for RNase H and for polymerase activity. Boyer, P.L., Gao, H.Q., Frank, P., Clark, P.K., Hughes, S.H. Virology (2001) [Pubmed]
  5. Specific contacts between mammalian U7 snRNA and histone precursor RNA are indispensable for the in vitro 3' RNA processing reaction. Cotten, M., Gick, O., Vasserot, A., Schaffner, G., Birnstiel, M.L. EMBO J. (1988) [Pubmed]
  6. Dynamic copy choice: steady state between murine leukemia virus polymerase and polymerase-dependent RNase H activity determines frequency of in vivo template switching. Hwang, C.K., Svarovskaia, E.S., Pathak, V.K. Proc. Natl. Acad. Sci. U.S.A. (2001) [Pubmed]
  7. Eukaryotic RNases H1 act processively by interactions through the duplex RNA-binding domain. Gaidamakov, S.A., Gorshkova, I.I., Schuck, P., Steinbach, P.J., Yamada, H., Crouch, R.J., Cerritelli, S.M. Nucleic Acids Res. (2005) [Pubmed]
  8. Increased levels of junB and c-jun mRNAs in male germ cells following testicular cell dissociation. Maximal stimulation in prepuberal animals. Alcivar, A.A., Hake, L.E., Hardy, M.P., Hecht, N.B. J. Biol. Chem. (1990) [Pubmed]
  9. Assessment of high-affinity hybridization, RNase H cleavage, and covalent linkage in translation arrest by antisense oligonucleotides. Gee, J.E., Robbins, I., van der Laan, A.C., van Boom, J.H., Colombier, C., Leng, M., Raible, A.M., Nelson, J.S., Lebleu, B. Antisense Nucleic Acid Drug Dev. (1998) [Pubmed]
  10. Role of RNase H in hybrid-arrested translation by antisense oligonucleotides. Walder, R.Y., Walder, J.A. Proc. Natl. Acad. Sci. U.S.A. (1988) [Pubmed]
  11. Relative contributions of Na+-dependent phosphate co-transporters to phosphate transport in mouse kidney: RNase H-mediated hybrid depletion analysis. Miyamoto, K., Segawa, H., Morita, K., Nii, T., Tatsumi, S., Taketani, Y., Takeda, E. Biochem. J. (1997) [Pubmed]
  12. Expression of mannose 6-phosphate receptor messenger ribonucleic acids in mouse spermatogenic and Sertoli cells. O'Brien, D.A., Welch, J.E., Fulcher, K.D., Eddy, E.M. Biol. Reprod. (1994) [Pubmed]
  13. Ribozyme-targeting procathepsin D and its effect on invasion and growth of breast cancer cells: An implication in breast cancer therapy. Vashishta, A., Ohri, S.S., Proctor, M., Fusek, M., Vetvicka, V. Int. J. Oncol. (2007) [Pubmed]
  14. A modified primer extension procedure for specific detection of DNA-RNA hybrids on nylon membranes. Kainz, P., Seifriedsberger, M., Strack, H.B. Anal. Biochem. (1989) [Pubmed]
  15. Enhanced activity of an antisense oligonucleotide targeting murine protein kinase C-alpha by the incorporation of 2'-O-propyl modifications. McKay, R.A., Cummins, L.L., Graham, M.J., Lesnik, E.A., Owens, S.R., Winniman, M., Dean, N.M. Nucleic Acids Res. (1996) [Pubmed]
  16. Rapid determination and quantitation of the accessibility to native RNAs by antisense oligodeoxynucleotides in murine cell extracts. Scherr, M., Rossi, J.J. Nucleic Acids Res. (1998) [Pubmed]
  17. Differential inhibition of DNA polymerase and RNase H activities of the reverse transcriptase by phosphonoformate. Margalith, M., Falk, H., Panet, A. Mol. Cell. Biochem. (1982) [Pubmed]
  18. Posttranscriptional regulation of thyrotropin beta-subunit messenger ribonucleic acid by thyroid hormone in murine thyrotrope tumor cells: a conserved mechanism across species. Staton, J.M., Leedman, P.J. Endocrinology (1998) [Pubmed]
  19. Multiple levels of regulation exist for expression of the Hoxa-4 (Hox-1.4) gene in the mouse testis. Viviano, C.M., Galliot, B., Wolgemuth, D.J. Cell. Mol. Biol. Res. (1993) [Pubmed]
  20. Stimulation of murine B lymphocytes induces a DNA exonuclease whose activity on switch-mu DNA is specifically inhibited by other germ-line switch region RNAs. Müller, J.R., Marcu, K.B. J. Immunol. (1998) [Pubmed]
  21. The location of the globin mRNA sequence within its 16S precursor. Smith, K., Rosteck, P., Lingrel, J.B. Nucleic Acids Res. (1978) [Pubmed]
  22. In male mouse germ cells, copper-zinc superoxide dismutase utilizes alternative promoters that produce multiple transcripts with different translation potential. Gu, W., Morales, C., Hecht, N.B. J. Biol. Chem. (1995) [Pubmed]
  23. T cell receptor-beta mRNA splicing during thymic maturation in vivo and in an inducible T cell clone in vitro. Qian, L., Vu, M.N., Carter, M.S., Doskow, J., Wilkinson, M.F. J. Immunol. (1993) [Pubmed]
  24. Epitope mapping of HIV-1 reverse transcriptase with monoclonal antibodies that inhibit polymerase and RNase H activities. Szilvay, A.M., Nornes, S., Haugan, I.R., Olsen, L., Prasad, V.R., Endresen, C., Goff, S.P., Helland, D.E. J. Acquir. Immune Defic. Syndr. (1992) [Pubmed]
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