Abstract
The in vivo function of p38 mitogen-activated protein kinase (MAPK) signaling in regulating the response to simulated microgravity is still largely unclear. Using Caenorhabditis elegans as an assay system, we investigated the in vivo function of p38 MAPK signaling in regulating the response of animals to simulated microgravity and the underlying molecular mechanism. Simulated microgravity treatment significantly increased the transcriptional expressions of genes (pmk-1, sek-1, and nsy-1) encoding core p38 MAPK signaling pathway and the expression of phosphorylated PMK-1/p38 MAPK. The pmk-1, sek-1, or nsy-1 mutant was susceptible to adverse effects of simulated microgravity. The intestine-specific activity of PMK-1 was required for its function in regulating the response to simulated microgravity, and the entire p38 MAPK signaling pathway could act in the intestine to regulate the response to simulated microgravity. In the intestine, SKN-1 and ATF-7, two transcriptional factors, were identified as downstream targets for PMK-1 in regulating the response to simulated microgravity. Therefore, the activation of p38 MAPK signaling may mediate a protection mechanism for nematodes against the adverse effects of simulated microgravity. Additionally, our results highlight the potential crucial role of intestinal cells in response to simulated microgravity in nematodes.
Highlights
It has been well known that spaceflight will lead to the formation of significant risk for human beings and animals, such as alterations in movement, muscle atrophy, and metabolism[5,6,7]
The control wild-type nematodes grown in liquid S medium showed the similar transcriptional expressions of genes encoding p38 mitogen-activated protein kinase (MAPK) signaling pathway to those in control wild-type nematodes grown on normal nematode growth medium (NGM) plates (Fig. S1a–c)
We observed the significant increase in transcriptional expressions of genes encoding the core p38 MAPK signaling pathway after simulated microgravity treatment (Fig. S1a–c)
Summary
It has been well known that spaceflight will lead to the formation of significant risk for human beings and animals, such as alterations in movement, muscle atrophy, and metabolism[5,6,7]. C. elegans is an ideal animal model for the study of physiological effects of simulated microgravity because of its common use on Earth as a model organism for human medical pathologies and its sensitivity to environmental toxicants or stresses[9,10,11]. The in vivo function of p38 MAPK signaling in the regulation of response to simulated microgravity and the underlying mechanism are still largely unclear. We determined the in vivo function of p38 MAPK signaling pathway in regulating the response to simulated microgravity in nematodes using rotary wall vessel bioreactor in Synthecon Rotary SystemTM. Our results will be helpful for our understanding the in vivo function of p38 MAPK signaling in the regulation of response of organisms to simulated microgravity
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