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Gene Review:

Rf1 - Renal disease susceptibility QTL 1

Rattus norvegicus

Van Dijk, S.J. et al., Vitt, U. et al., Yu, H. et al., Provoost, A.P. et al., Brown, D.M. et al., et al.

Provoost, Shiozawa, Van Dokkum, Jacob, Van Dijk, Specht, Lazar, Jacob, Provoost, Vitt, Gietzen, Stevens, Wingrove, Becha, Bulloch, Burrill, Chawla, Chien, Crawford, Ison, Kearney, Kwong, Park, Policky, Weiler, White, Xu, Daniels, Jacob, Jensen-Seaman, Lazar, Stuve, Schmidt,

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Disease relevance of Rf1

As an example, we have used the syntenic information for the rat Rf-1 disease region and the orthologous human ESRD disease region to reduce the size of the original rat QTL to only 11.5 Mb [1].
BACKGROUND:Linkage analyses of crosses of rats susceptible to renal damage, fawn-hooded hypertensive (FHH), and those resistant to kidney damage, August x Copenhagen Irish (ACI), indicated that five quantitative trait loci (QTLs), Rf-1 to Rf-5, influence proteinuria (UPV), albuminuria (UAV) and focal glomerulosclerosis (FGS) [2].
Two renal failure susceptibility genes, Rf-1 and Rf-2, have been identified in the fawn-hooded rat, an animal model of hypertension and nephrosclerosis [3].

High impact information on Rf1

Here, we report the localization of two genes, Rf-1 and Rf-2, responsible for about half of the genetic variation in key indices of renal impairment [4].
Rf-1 strongly affects the risk of renal impairment, but has no significant effect on blood pressure [4].
Using the syntenic information in combination with expression data from ESTs and microarrays, we have selected a set of 66 candidate disease genes for Rf-1 [1].
In an (E3 x DA)F(2) cohort a major locus controlling the levels of IgM-RF in serum was identified on chromosome 11 (Rf1) and another on chromosome 16 (Rf3), and these were not related to arthritis susceptibility [5].
BACKGROUND: Five quantitative trait loci (QTLs), Rf-1 to Rf-5, were found in Fawn-Hooded hypertensive (FHH) rats influencing susceptibility to renal damage [6].

Biological context of Rf1

To study the impact of Rf-1 in the absence of the other loci, we transferred the Rf-1 region of chromosome 1, between the markers D1Mit34 and D1Rat156, Rf-1B for short, onto the genomic background of the normotensive August x Copenhagen Irish (ACI) rat [7].
The Rf-1 QTL carries one or more genes impairing renal autoregulation and influencing renal damage susceptibility [2].
Evaluation of markers on human chromosome 10, including the homologue of the rodent Rf-1 gene, for linkage to ESRD in black patients [3].

References

Identification of candidate disease genes by EST alignments, synteny, and expression and verification of Ensembl genes on rat chromosome 1q43-54. Vitt, U., Gietzen, D., Stevens, K., Wingrove, J., Becha, S., Bulloch, S., Burrill, J., Chawla, N., Chien, J., Crawford, M., Ison, C., Kearney, L., Kwong, M., Park, J., Policky, J., Weiler, M., White, R., Xu, Y., Daniels, S., Jacob, H., Jensen-Seaman, M.I., Lazar, J., Stuve, L., Schmidt, J. Genome Res. (2004) [Pubmed]
Renal damage susceptibility and autoregulation in RF-1 and RF-5 congenic rats. Van Dijk, S.J., Specht, P.A., Lazar, J., Jacob, H.J., Provoost, A.P. Nephron Exp. Nephrol. (2005) [Pubmed]
Evaluation of markers on human chromosome 10, including the homologue of the rodent Rf-1 gene, for linkage to ESRD in black patients. Yu, H., Sale, M., Rich, S.S., Spray, B.J., Roh, B.H., Bowden, D.W., Freedman, B.I. Am. J. Kidney Dis. (1999) [Pubmed]
Renal disease susceptibility and hypertension are under independent genetic control in the fawn-hooded rat. Brown, D.M., Provoost, A.P., Daly, M.J., Lander, E.S., Jacob, H.J. Nat. Genet. (1996) [Pubmed]
The genetic control of rheumatoid factor production in a rat model of rheumatoid arthritis. Wernhoff, P., Olofsson, P., Holmdahl, R. Arthritis Rheum. (2003) [Pubmed]
Interaction between Rf-1 and Rf-4 quantitative trait loci increases susceptibility to renal damage in double congenic rats. Van Dijk, S.J., Specht, P.A., Lutz, M.M., Lazar, J., Jacob, H.J., Provoost, A.P. Kidney Int. (2005) [Pubmed]
Transfer of the Rf-1 region from FHH onto the ACI background increases susceptibility to renal impairment. Provoost, A.P., Shiozawa, M., Van Dokkum, R.P., Jacob, H.J. Physiol. Genomics (2002) [Pubmed]

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