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. Author manuscript; available in PMC: 2017 Jun 7.
Published in final edited form as: Sci Signal. 2016 Jun 7;9(431):ra59. doi: 10.1126/scisignal.aad3373

Fig. 8. S37A mutation of GATA6L mimics and competes with the repression of transcript abundance in the TNF-insulin crosstalk cluster.

Fig. 8

(A) Doxycycline-inducible overexpression of WT GATA6L in HT-29 cells. Cells were treated with doxycycline (1 μg/ml) for 24 hours. (B) Ratio of TNF-induced transcript abundance for crosstalk cluster genes in the presence or absence of GATA6L overexpression. Data are mean ratios of n = 3 independent biological samples assessed by microarray profiling, with bias in the ratio assessed by two-sided binomial test. (C) S37A mutation of GATA6L mimics insulin stimulation (green) and antagonizes TNF-insulin crosstalk (purple). qRT-PCR data for cluster #9 genes in WT and S37A mutant (S37A) GATA6L addback cells pretreated with IFNγ and stimulated with TNF, insulin, or both for 2 or 4 hours. Data are row-standardized geometric means of n = 6 biological replicates across two separate experiments, with interactions between GATA6 status and TNF or insulin assessed by log-transformed five-way ANOVA with the following factors: GATA6, transcript, TNF, insulin, and time. (D) Three-state conceptual model for GATA6L regulation by TNF and insulin and its relation to the crosstalk cluster of transcripts. Ovals annotate the figure subpanels supporting the links depicted.