Podocyte-specific expression of Cre recombinase in transgenic mice

被引:269
作者
Moeller, MJ
Sanden, SK
Soofi, A
Wiggins, RC
Holzman, LB
机构
[1] Univ Michigan, Sch Med, Dept Internal Med, Div Nephrol, Ann Arbor, MI 48109 USA
[2] Dept Vet Affairs, Ann Arbor, MI USA
关键词
kidney; podocin; glomerulus;
D O I
10.1002/gene.10164
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
We report a transgenic mouse line that expresses Cre recombinase exclusively in podocytes. Twenty-four transgenic founders were generated in which Cre recombinase was placed under the regulation of a 2.5-kb fragment of the human NPHS2 promoter. Previously, this fragment was shown to drive beta-galactosidase (P-gal) expression exclusively in podocytes; of transgenic mice. For analysis, founder mice were bred with ROSA26 mice, a reporter line that expresses P-gal in cells that undergo Cre recombination. Eight of 24 founder lines were found to express P-gal exclusively in the kidney. Histological analysis of the kidneys showed that P-gal expression was confined to podocytes. Cre recombination occurred during the capillary loop stage in glomerular development. No evidence for Cre recombination was detected in any of 14 other tissues examined. (C) 2002 Wiley-Liss, Inc.
引用
收藏
页码:39 / 42
页数:4
相关论文
共 14 条
[1]   NPHS2, encoding the glomerular protein podocin, is mutated in autosomal recessive steroid-resistant nephrotic syndrome [J].
Boute, N ;
Gribouval, O ;
Roselli, S ;
Benessy, F ;
Lee, H ;
Fuchshuber, A ;
Dahan, K ;
Gubler, MC ;
Niaudet, P ;
Antignac, C .
NATURE GENETICS, 2000, 24 (04) :349-354
[2]  
Cushman LJ, 2000, GENESIS, V28, P167, DOI 10.1002/1526-968X(200011/12)28:3/4<167::AID-GENE120>3.0.CO
[3]  
2-N
[4]  
Eremina V, 2002, J AM SOC NEPHROL, V13, DOI 10.1681/ASN.V133788
[5]   Positionally cloned gene for a novel glomerular protein - nephrin - is mutated in congenital nephrotic syndrome [J].
Kestila, M ;
Lenkkeri, U ;
Mannikko, M ;
Lamerdin, J ;
McCready, P ;
Putaala, H ;
Ruotsalainen, V ;
Morita, T ;
Nissinen, M ;
Herva, R ;
Kashtan, CE ;
Peltonen, L ;
Holmberg, C ;
Olsen, A ;
Tryggvason, K .
MOLECULAR CELL, 1998, 1 (04) :575-582
[6]   Podocyte depletion and glomerulosclerosis have a direct relationship in the PAN-treated rat [J].
Kim, YH ;
Goyal, M ;
Kurnit, D ;
Wharram, B ;
Wiggins, J ;
Holzman, L ;
Kershaw, D ;
Wiggins, R .
KIDNEY INTERNATIONAL, 2001, 60 (03) :957-968
[7]   Progression of glomerular diseases: Is the podocyte the culprit? [J].
Kriz, W ;
Gretz, N ;
Lemley, KV .
KIDNEY INTERNATIONAL, 1998, 54 (03) :687-697
[8]  
Moeller MJ, 2000, J AM SOC NEPHROL, V11, P2306, DOI 10.1681/ASN.V11122306
[9]   Two gene fragments that direct podocyte-specific expression in transgenic mice [J].
Moeller, MJ ;
Sanden, SK ;
Soofi, A ;
Wiggins, RC ;
Holzman, LB .
JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY, 2002, 13 (06) :1561-1567
[10]   Rearrangements of the cytoskeleton and cell contacts induce process formation during differentiation of conditionally immortalized mouse podocyte cell lines [J].
Mundel, P ;
Reiser, J ;
Borja, AZM ;
Pavenstadt, H ;
Davidson, GR ;
Kriz, W ;
Zeller, R .
EXPERIMENTAL CELL RESEARCH, 1997, 236 (01) :248-258