Salk Institute scientists report in the journal Science that the type of mothering a female mouse provides her pups actually changes their DNA. The work lends support to studies about how childhood environments affect brain development in humans and could provide insights into neuropsychiatric disorders such as depression and schizophrenia.
According to Salk, most cells in the mammalian brain undergo changes to their DNA that make each neuron slightly different from its neighbor. Some of these changes are caused by “jumping” genes—known as long interspersed nuclear elements (LINEs)—that move from one spot in the genome to another. In 2005, Salk scientist Rusty Gage and his team discovered that a jumping gene called L1, which was already known to copy and paste itself into new places in the genome, could jump in developing neuronal brain cells.
As reported in Science, the team recently discovered a correlation between maternal care and L1 copy number: Mice with attentive mothers had fewer copies of the jumping gene L1, and those with neglectful mothers had more L1 copies, and thus more genetic diversity in their brains. Further research showed that mice with neglectful mothers had noticeably fewer methylated L1 genes than those with attentive mothers, suggesting that methylation is the mechanism responsible for the mobility of the L1 gene.
TIME’s powerful series, “TIME Firsts: Women Who Are Changing the World,” profiles Salk Institute President Elizabeth Blackburn, the first woman president of the institute. Blackburn won the 2009 Nobel Prize in Physiology or Medicine for discovering the molecular nature of telomeres, the ends of chromosomes that serve as protective caps essential for preserving genetic information, and for co-discovering telomerase, an enzyme that maintains telomere ends. Both telomeres and telomerase are thought to play central roles in aging and diseases such as cancer, and her work helped launch entire new fields of research in these areas. Blackburn has been president of the Salk Institute since January 2016.
Supported by the NOMIS Foundation and the Glenn Center for Aging Research, researchers at the Salk Institute probing the premature aging disorder Hutchinson-Gilford progeria have uncovered an errant protein process in the disease that could help healthy people as well as progeria sufferers live longer.
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Susan Kaech, currently professor of Immunobiology at Yale University, will join Salk as NOMIS Foundation Chair and director of the NOMIS Center for Immunobiology and Microbial Pathogenesis beginning in 2018. Kaech studies how immune cells — called T cells — remember infectious agents our bodies have previously encountered in order to mount a more rapid response the next time we’re exposed to them.
In her current position as Waldemar Von Zedtwitz Professor of Immunobiology at Yale University, she has studied T cell memory in the context of vaccine effectiveness, chronic viral infections and immune system suppression by cancer. Her lab has been a leader in elucidating the mechanisms responsible for T cell memory and, as part of the rapidly advancing field of cancer immunotherapy, Kaech is studying ways of harnessing the immune system to attack tumors.
Kaech is a recipient of numerous prestigious awards including the Howard Hughes Medical Institute Early Career Scientist award, the Presidential Early Career Award for Scientists and Engineers, the Edward Mallinckrodt Jr. award and the Burroughs-Wellcome Foundation award. She has been named an investigator of the American Asthma Foundation and the Cancer Research Institute. Kaech received her PhD from Stanford University and her BS from the University of Washington in Seattle.
“The research that people are doing at Salk is spectacular — really cutting-edge — and the tools that the labs are using to answer questions are very powerful and exciting,” says Kaech. “I hope that being at Salk will push me to think about problems in a different manner or with different technologies that may ultimately lead to new understandings or new ways of thinking about the function of our immune system.”