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. 2019 May 24;33(8):9516–9525. doi: 10.1096/fj.201900428RR

Figure 2.

Figure 2

Infection activates the ER stress response, followed by autophagy and production of lipid droplets. Salubrinal (SAL) lowers production of lipid droplets but not production of viral NP. A) Infection by virus causes MDCK cells to increase expression of calreticulin, an indicator of ER stress, within 3 HPI and peaking by 6 HPI. Increase in LC3-I (18 kD) and its conversion to LC3-II (16 kD) occurs later, becoming detectable by 6 HPI and peaking by 10 HPI. β-Tubulin is a loading control. B, C) SAL (100 μM), an inhibitor of the PERK pathway of ER stress, suppresses the lipid response in a dose-dependent manner. SAL, likewise, partially though not completely suppresses the formation of lipid droplets [P < 0.01 between infected (I) and infected, SAL-treated (I+SAL) cells]. D) Nevertheless, SAL does not prevent the formation of NP. Note: In this and other figures, the intensity of NP may be compared with that shown in Figs. 4 and 5, as the entire NP series illustrated is one of 3 separate series run. In all micrographs, the original magnification is ×400 and the full field is shown.