These results suggest that glucose deprivation, but not amino acids deprivation or hypoxia, promotes ER stress in HRCCs in culture.
We have demonstrated that glucose deprivation, not hypoxia and amino acids shortage induces ER stress and activates the IRE1 and PERK pathways in human renal cortical cells (HRCCs) in culture.
In D. dadantii EC16, the Hrp system appears to contribute to an early stage of pathogenesis, whereas in D. dadantii 3937 mutation of hrpN, hrpG, and hrcC resulted in substantially reduced lesion formation and bacterial growth in African violet leaves [ 26, 27].
Three mutants were analyzed, prtE, outC and hrcC impaired in type I, II and III secretion systems respectively (Fig. 1A).
Together, these results indicate that metabolic stress activates IRE1 signaling in HRCCs.
To produce metabolic stress, HRCCs were incubated in a nutrient-deprived culture medium.
These results suggest that metabolic stress activates the PERK pathway in HRCCs.
In HRCCs subjected to metabolic stress, the transcriptional factor X-box-binding protein 1 (XBP1) was actively spliced during glucose deprivation, suggesting that IRE1 is activated during metabolic stress.
The cell-associated proteins HrcC and WesC were more abundant at 18°C in UW551 (group 8 in Table 2), supporting a role in virulence at low temperature.
tomato DC3000 and its hrcC derivative strain were cultivated at 30°C in LB medium.
