Fig. 3

Inhibition of Fgf signaling prevents new nephron development. (A) Injured zebrafish generate lhx1a ?+ ?nephrogenic aggregates at 7 dpi by whole mount in situ hybridization. (B) Treatment with the FGFR1 inhibitor PD166866 blocks the appearance of lhx1a ?+ ?nephrogenic aggregates in whole mount kidneys. (C) Quantification of lhx1a ?+ ?nephrogenic aggregates in multiple whole mount kidneys demonstrates PD166866 completely blocks kidney regeneration. N ?= ?7 fish per condition. Error bars indicate ±SD. p ?= ?0.01 by Mann-Whitney T-test. (D) qRTPCR quantitation of lhx1a expression shows PD166866 treatment blocks lhx1a expression post-injury. N ?= ?6 fish per condition. Error bars indicate ±SD. * indicates p ?= ?0.02 by Kruskal-Wallis test. (E) Control non-heat shocked Tg(hsp70:dnfgfr1) transgenic fish show lhx1a ?+ ?new nephron aggregates 7 days following gentamicin injury. (F) Heat shock induction of the dominant-negative Fgfr1 receptor blocked the development of lhx1a ?+ ?new nephron aggregates. (G) Quantification of lhx1a ?+ ?nephrogenic aggregates in multiple whole mount kidneys demonstrates that expression of the dominant-negative Fgfr1 receptor completely blocks kidney regeneration. Differences in injury responses (number of nephrogenic aggregates in A vs E) reflect strain dependent differences in sensitivity to gentamicin injury. N ?= ?4 control and N ?= ?5 heat shocked fish. Error bars indicate ±SD. p ?= ?0.03 by Mann-Whitney T-test. In panels A,B,E,F scale bars are 100 ??m.