October 30, 2015
Science Daily/University of Tennessee at Knoxville
Lack of adequate sleep can do more than just make you tired. It can short-circuit your system and interfere with a fundamental cellular process that drives physical growth, physiological adaptation and even brain activity, according to a new study.

Albrecht von Arnim, a molecular biologist based in the Department of Biochemistry and Cellular and Molecular Biology, studied plants but said the concepts may well translate to humans.

His team examined how protein synthesis--the process that determines how organisms grow and how cells renew themselves--changes over the course of the daily day-night cycle. He also explored whether any such changes are controlled by the organism's internal time keeper, the circadian clock.

Proteins are newly created in every cell by translating messages made from the cell's own DNA, the genome.

Von Arnim's findings, published in the journal Plant Cell, show not only that protein synthesis activity changed over the course of the day, but also that it was under the influence of the circadian clock.

"When we misalign our behavior with our circadian clock, for example by creating jet lag, or by working as a night owl, we do not only disrupt normal physiological processes such as cycles of appetite and body temperature," von Arnim said. "This work in plants suggests that we may also be interfering with a more fundamental cellular process, protein synthesis."

Muscle action, brain activity, growth and development are functions all performed by proteins whose synthesis is carefully regulated, he said. "For example, when cells are stressed by high temperatures or from a virus infection, they drastically reduce their protein synthesis activity," von Arnim said.

The findings could also have implications for agricultural production as farmers and companies seek to better cultivate land and maximize outputs from plants required to sustain human life.

"Protein synthesis is part of the basis for crop yield," von Arnim said.
http://www.sciencedaily.com/releases/2015/10/151030153115.htm