Abstract
Extracellular signal-regulated protein kinase 1 and 2 (ERK1/2) are members of the MAPK family and participate in the transduction of stimuli in cellular responses. Their long-term actions are accomplished by promoting the expression of specific genes whereas faster responses are achieved by direct phosphorylation of downstream effectors located throughout the cell. In this study we determined that hERK1 translocates to the mitochondria of HeLa cells upon a proliferative stimulus. In the mitochondrial environment, hERK1 physically associates with (i) at least 5 mitochondrial proteins with functions related to transport (i.e. VDAC1), signalling, and metabolism; (ii) histones H2A and H4; and (iii) other cytosolic proteins. This work indicates for the first time the presence of diverse ERK-complexes in mitochondria and thus provides a new perspective for assessing the functions of ERK1 in the regulation of cellular signalling and trafficking in HeLa cells.
Highlights
ERK1 and ERK2 are members of the MAPK family of signalling proteins and play key roles in the transduction of extracellular stimuli into cellular responses [1,2]
In this work we demonstrated the presence of endogenous and recombinant hERK1 in purified non-contaminated mitochondria of HeLa cells
HeLa cells were transfected with hERK1-GFP and further stained with a specific mitochondrial marker, MitoTracker RED CMXRos, and analyzed by confocal microscopy
Summary
ERK1 and ERK2 are members of the MAPK family of signalling proteins and play key roles in the transduction of extracellular stimuli into cellular responses [1,2]. Induction of this signalling cascade leads to the phosphorylation of several target proteins that regulate cellular fate and other physiological processes [3]. While recent evidence suggests that the ERK kinases are not functionally redundant and may have very different roles [see 8 for review], further studies are needed to assess the interplay between the two proteins and its effects on signalling dynamics. Poderoso et al [5] observed that ERK1/2 activation by cAMP results in maximal steroidogenic rate
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