While it primarily works to protect cells, autophagy can also contribute to cell death. Researchers at Sweden’s Karolinska Institutet this week pinpoint a particular histone modification that they say regulates the outcome of autophagy.

H4K16 deacetylation, the researchers report, is predominantly associated with the down-regulation of autophagy-related genes. Antagonizing H4K16 down-regulation upon autophagy induction, the Karolinska team found, promotes cell death.

“Our findings establish that alteration in a specific histone post-translational modification during autophagy affects the transcriptional regulation of autophagy-related genes and initiates a regulatory feedback loop, which serves as a key determinant of survival versus death responses upon autophagy induction,” the researchers write in a paper published online in Nature this week.

In a statement, Karolinska’s Bertrand Joseph, Ph.D., noted the importance of autophagy in human disease. “All we have to do is select a disease model and test whether there’s anything to be gained from influencing the new signal network that we’ve identified,” he said.

“Our findings open up avenues for influencing autophagy,” Dr. Joseph added.

“The histone H4 lysine 16 acetyltransferase hMOF regulates the outcome of autophagy” appeared online in Nature July 17.

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