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. 2015 May 15;26(10):1947–1956. doi: 10.1091/mbc.E14-11-1497

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© 2015 ErLin et al. This article is distributed by The American Society for Cell Biology under license from the author(s). Two months after publication it is available to the public under an Attribution–Noncommercial–Share Alike 3.0 Unported Creative Commons License (http://creativecommons.org/licenses/by-nc-sa/3.0).

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FIGURE 7: — p-ERK1/2 is activated by stress formation and is critical for protection against apoptosis. (A) p-ERK1/2 was activated in the cytoplasm of Sertoli cells (black arrows) after heat treatment. Scale bars: 40 μm. (B) ERK1/2 was phosphorylated as long as stress granules were formed upon treatment with various stress granule stimulators, including heat stress, NaAsO₂, and MG132. (C) The formation of stress granules in Sertoli cells was not affected by inhibiting ERK1/2 phosphorylation using the specific inhibitor U0126. (D) The percentage of apoptotic Sertoli cells is counted from each treated group, based on the TUNEL staining. Each bar represents the mean ± SD of n = 3 experiments. *, p < 0.05. (E) p-ERK1/2 was not activated in Msi-1–silenced Sertoli cells upon heat treatment. (F) Schematic presentation of two distinct roles of Msi-1 in the BTB regulation and Sertoli cell fate upon heat stress.