FIGURE

Figure 5

ID
ZDB-FIG-250109-276
Publication
Dai et al., 2024 - Hyperaminoacidemia from interrupted glucagon signaling increases pancreatic acinar cell proliferation and size via mTORC1 and YAP pathways
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Figure 5

IGS activates the YAP/Taz pathway

(A) Upregulation of YAP target genes in acinar cells from GCGR-Ab treated mice. Data are from RNA-seq.

(B) RT-qPCR analysis of selected YAP target genes in mRNA from the pancreas of IgG and GCGR-Ab treated mice (n = 4–5/group, compared IgG vs. GCGR-Ab each gene).

(C and E) Representative immunofluorescence images of YAP (red) in acinar cells (amylase, green) in the two mouse models. Arrows point to a high expression of YAP. Scale bar, 50 μm.

(D and F) Quantifications of the percentage of acinar cells with high YAP expression (n = 5/group). p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001 Student’s t test.

(G) Representative immunofluorescence images of Yap in pancreas sections of WT, gcgr−/−, and gcgr−/− with slc38a5b knockdown, and gcgr−/− with rapamycin treatment. All fish carry Tg(ela3l:EGFP) transgene that labels acinar cells with EGFP (scale bar, 10 μm). The EGFP- cells with high Yap1 signal are likely ductal cells.

(H) Quantification of the percentage of acinar cell with nuclear Yap1. n = 7, 6, and 7 for each group, respectively. Data are represented as mean ± SEM. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001. One-way ANOVA followed by Tukey’s multiple comparisons test.

Expression Data
Gene:
Fish:
Condition:
Knockdown Reagents:
Anatomical Terms:
Stage: Adult

Expression Detail
Antibody Labeling
Phenotype Data
Fish:
Condition:
Knockdown Reagents:
Observed In:
Stage: Adult

Phenotype Detail
Acknowledgments
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