Bolar et al., 2016 - Heterozygous Loss-of-Function SEC61A1 Mutations Cause Autosomal-Dominant Tubulo-Interstitial and Glomerulocystic Kidney Disease with Anemia. American journal of human genetics   99:174-187 Full text @ Am. J. Hum. Genet.

Fig. 6

Suppression of SEC61A1 Leads to Pronephric Tubular Atrophy in Zebrafish

(A-C) Whole-mount immunostaining of 4 days post-fertilization (dpf) zebrafish larvae with anti-Na+/K+-ATPase alpha subunit monoclonal antibody (±6F) shows the overall anatomy of the pronephric ducts (pd) and pronephric tubules (pt), which become progressively convoluted in control larvae. Three levels of convolution were assessed: convoluted (normal) (A and A′), V-shaped (B and B′), and straight pronephric tubule (C and C′). The pronephric ducts are normal.

(D) Qualitative scoring of the tubular atrophy was performed in larvae batches injected with sec61al2 MO alone; MO and mutant (p.Thr185Ala) RNA or (p.Val67Gly) RNA; MO and wild-type (WT) capped-RNA; WT and mutant RNAs alone; and control.

(E) Results of Fisher’s exact test conducted between pairs of conditions. The significant p values (< 0.05) are highlighted in red.

PHENOTYPE:
Fish:
Knockdown Reagent:
Observed In:
Stage: Day 4

Fig. S7 ZFIN is incorporating published figure images and captions as part of an ongoing project. Figures from some publications have not yet been curated, or are not available for display because of copyright restrictions.

PHENOTYPE:
Fish:
Knockdown Reagent:
Observed In:
Stage: Day 4
Acknowledgments:
ZFIN wishes to thank the journal American journal of human genetics for permission to reproduce figures from this article. Please note that this material may be protected by copyright. Full text @ Am. J. Hum. Genet.