FIGURE

Fig. 6

ID

ZDB-FIG-160511-12

Publication

DeRossi et al., 2016 - trappc11 is required for protein glycosylation in zebrafish and humans

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Fig. 6

Atorvastatin is synthetically lethal with trappc11 mutation. (A) Transgenic WT and trappc11-mutant embryos expressing a liver-specific marker (Tg(fabp10:dsRed)) were treated with DMSO or the HMG-CoA reductase inhibitor, Atv, between 3 and 5 dpf at the concentrations indicated and analyzed for gross morphology and lethality. (B) Livers were collected from WT (n = 7 clutches), trappc11 (n = 8 clutches), and 5 µM Atv–treated WT embryos between 3 and 5 dpf (n = 7 clutches) and subjected to qPCR to analyze UPR gene expression used to calculate PC1. p values were calculated with Student’s t test. n.s., not significant. (C) Livers from larvae treated with DMSO or 1 µM Atv from 3 to 5 dpf (n = 8 clutches) were collected and analyzed at 5 dpf for the expression of genes involved in N-linked glycosylation. Atorvastatin-induced fold increases are shown relative to DMSO-treated samples.

Expression Data

Genes:	alg2 alg5 alg9 dpagt1 gmppb hmgcs1 pmm2
Fish:	AB/TU
Condition:	chemical treatment: atorvastatin
Anatomical Term:	liver
Stage:	Day 5

Expression Detail

Antibody Labeling

Phenotype Data

Fish:	AB/TU trappc11^{hi1532bTg/hi1532bTg}; gz15Tg
Condition:	chemical treatment: atorvastatin
Observed In:	liver response to endoplasmic reticulum stress whole organism
Stage:	Day 5

Phenotype Detail

Acknowledgments

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