FIGURE

Fig. 7

ID

ZDB-FIG-171129-8

Publication

Hoodless et al., 2016 - Genetic and pharmacological inhibition of CDK9 drives neutrophil apoptosis to resolve inflammation in zebrafish in vivo

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Fig. 7

Knockdown of LaRP7 increases inflammation at the wounded tailfin, and this can be inhibited using the CDK inhibitor AT7519.

(a) Tg(mpx:EFGP)ⁱ¹¹⁴ zebrafish eggs were injected with a mismatched control or a morpholino sequence to knockdown LaRP7, and at 3 dpf the tailfin was transected with representative images at 24 hpi shown [i, ii]. (b) Neutrophils at the wounded tailfin [i] and also in the whole embryo [ii] were quantified. ≥10 fish per group in 3 independent experiments. (c) LaRP7 knockdown and control zebrafish were also injected with AT7519/DMSO at 4 hpi and the neutrophils quantified at various time points; shown is the 24 hpi time point. ≥19 fish per group in 3 independent experiments. Data shown as ±S.E.M. *p < 0.05. n/s: not significant. Data analysed by two-way ANOVA followed by post-hoc Newman Keuls or unpaired t-test.

Expression Data

Gene:	GFP
Fish:	i114Tg i114Tg + MO2-larp7
Condition:	transection: caudal fin
Knockdown Reagent:	MO2-larp7
Anatomical Term:	neutrophil
Stage:	Day 4

Expression Detail

Antibody Labeling

Phenotype Data

Fish:	i114Tg i114Tg + MO2-larp7
Conditions:	chemical treatment by injection: 4-(2,6-dichlorobenzamido)-N-(piperidin-4-yl)-pyrazole-3-carboxamide, transection: caudal fin transection: caudal fin
Knockdown Reagent:	MO2-larp7
Observed In:	regenerating fin neutrophil whole organism neutrophil
Stage:	Day 4

Phenotype Detail

Acknowledgments

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