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When it comes to protecting cells from death brought on by the
calamities of environmental stress, the human body is particularly
ingenious. From cellular components that suck up misfolded proteins to a
vigilant immune system, the ways we protect our cells (and ourselves)
are many and mysterious.
Scientists from the Florida campus of The Scripps Research Institute
(TSRI) have now uncovered the workings of another cell-protection
device, one that may play a major role in a number of age-related
diseases, including diabetes and Parkinson’s, Alzheimer’s and
Huntington’s diseases.
The study, led by Srinivasa Subramaniam, a TSRI assistant professor,
and Solomon H. Snyder, a neuroscience professor at Johns Hopkins
University School of Medicine, was published February 5 in the journal
Cell Reports.
More or Less Acceleration
The study focuses on a new pathway through which Rheb, a regulator
that many believe is active in the brain’s ability to change in response
to learning, actually plays two roles, rather than one—stimulating and
inhibiting protein synthesis.
The interplay between the two roles may be the key that enables cells
to alter protein synthesis and protect the cell in response to varying
environmental stresses.
“We found Rheb acts like the gas pedal in a car,” Subramaniam said.
“It can either increase translation or decrease it. And because
translation is a fundamental process that is affected in a lot of
diseases, we now think that Rheb may act like a switch in some disease
states—helping to turn them off and on.”
Rheb is known to bind and activate mTOR, a developmentally important
gene that integrates signals from multiple pathways and regulates
critical cell functions such as protein synthesis. Besides its role as
an activator of mTOR, which plays a major role in conditions from
diabetes to neurodegenerative disease, the mTOR-independent role of Rheb
is less known. The new study defines crucial mTOR-independent effects
of Rheb. Results showed that, when stressed, Rheb instead inhibits
protein synthesis by amplifying the phosphorylation (adding a phosphate
group to a protein to alter its function) of another protein known
eIF2a. As a result, cell resources can be conserved rather than
squandered when the environment is challenging.
“We don’t really understand the full role of the Rheb-mTOR pathway,
but we have uncovered a new fundamental process of Rheb that is
independent of mTOR and very intriguing,” said Neelam Shahani, a member
of Subramaniam’s lab who was co-first author of the study with Richa
Tyagi of Johns Hopkins University School of Medicine. “Rheb can inhibit
protein synthesis, and we know that protein misfolding via environmental
stress factors is present in a lot of diseases.”
Subramaniam noted that, intriguingly, an earlier study had suggested
the Rheb pathway had been implicated in Alzheimer’s disease. “We also
want to look at Rheb’s role in other neurodegenerative diseases,” he
said.
In addition to Subramaniam, Snyder, Shahani and Tyagi, authors of the
study, “Rheb Inhibits Protein Synthesis by Activating the PERK-eIF2α
Signaling Cascade,” include Max Ferretti, William Pryor, Supriya
Swarnkar and Katrin Karbstein of TSRI; Lindsay Gorgen of Florida
Atlantic University; as well as Paul F. Worley and Po Yu Chen of Johns
Hopkins University School of Medicine.
This work was supported by the State of Florida, the O'Keeffe
Neuroscience Scholar Award and the United States Public Health Service
(DA000266).
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