Fig. 3: aux-depleted ECs undergo ERS-induced apoptosis. | Cell Death & Disease

Fig. 3: aux-depleted ECs undergo ERS-induced apoptosis.

From: Auxilin in enterocytes controls intestinal homeostasis through inter-cell communication

Fig. 3

A Compared to control intestines in which apoptosis (by GC3Ai, green) is barely detectable, the number of GC3Ai+ cells (white arrowheads) is significantly increased in Myo1Ats>auxRNAi intestines at 29 °C for 3 days. Quantification of GC3Ai+ cell No/image in control and Myo1Ats>auxRNAi intestines. Mean ± SD is shown. ****p < 0.0001. B Simultaneous expression of p35 almost completely rescued the defects observed in Myo1Ats>auxRNAi intestines at 29 °C for 7 days (by esg-lacZ, red, white arrowheads). Quantification of esg-lacZ+ cell No/images in different genotypes indicated. Mean ± SD is shown. ****p < 0.0001. C Compared to ECs in control intestines in which ER stress (by Hsc3, red, white arrowheads) is barely detectable, Hsc3 is dramatically increased in Myo1Ats>auxRNAi intestines at 29 °C for 3 days. Please note that ER stress is constantly occurred in some EEs (yellow arrowheads) in control and Myo1Ats>auxRNAi intestines. Hsc3 channel is showed separately in black white. Quantification of the fluorescence intensity of Hsc3 in ECs of control and Myo1Ats>auxRNAi intestines. Mean ± SD is shown. ****p < 0.0001. D Compared to control intestines in which Xbp1-GFP (white arrowhead) is barely detectable, Xbp1-GFP is significantly increased in Myo1Ats>auxRNAi intestines at 29 °C for 3 days. Xbp1-GFP channel is showed separately in black white. Quantification of the fluorescence intensity of Xbp1-GFP in control and Myo1Ats>auxRNAi intestines. Mean ± SD is shown. ****p < 0.0001. Scale bars, 5 μm (C, 20 μm).

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