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Basic Briefs

Why Only Mothers Pass Mitochondrial DNA to Their Children

By Jill Adams | Illustrations by Matt Chinworth

Mitochondria, which produce energy for cellular functions, have their own genome — and we all inherit our mitochondrial DNA entirely from our mothers. Researchers theorize that if maternal and paternal mitochondrial DNA both ended up in a fertilized egg, they would compete in ways that are detrimental. However, the precise mechanisms behind the loss of paternal mitochondrial DNA have not been elucidated — until now.

Biochemist Dmitry Temiakov, PhD, and colleagues, used a sensitive method to detect DNA in sperm and showed that mature sperm do not carry any intact mitochondrial DNA. Dr. Temiakov’s team looked for clues by exploring molecular pathways involved in sperm maturation. They identified a specific protein called mitochondrial transcription factor A, or TFAM. In most other cells, TFAM serves as a helper molecule for mitochondrial DNA, but during sperm generation, the protein is modified and is unable to gain entry into mitochondria. Without TFAM, the genetic material in mitochondria is unprotected from degradation, and thus, mature sperm are left without any mitochondrial DNA.

“Nature ensures maternal mitochondrial DNA inheritance,” Dr. Temiakov says. “There are likely multiple pathways to prevent the transmission of paternal mitochondrial DNA. We have uncovered one of them.” While the discovery is exciting, he adds that there is much more to learn. Dr. Temiakov’s work earned the 2023 Michael and Melina Pellini Award for Innovation in the Biomedical Sciences.

Studying Inflammation in Multiple Sclerosis

By Moriah Cunningham  | Illustrations by Matt Chinworth

Nearly three million people worldwide suffer from multiple sclerosis (MS). The disease is a result of immune cells attacking a patient’s own brain cells, leading to symptoms that include vision loss, decreased muscle strength and sensory issues. Relapsing-remitting MS (RRMS) is the most common form of MS, whereby patients have flare-ups followed by periods of remission.

Neurology researcher Silva Markovic-Plese, MD, PhD, and her team have been studying RRMS for more than a decade. They had previously found elevated levels of an immune chemical called IL-11 in the cerebrospinal fluid surrounding the brain and spinal cord of RRMS patients. They wanted to explore why.

In the current study, researchers found that IL-11 promotes migration of inflammatory cells to the brain, which contributes to disease progression of RRMS. When they reduced the IL-11 levels in mice, they found lower levels of inflammation and disease progression compared to controls.

“Although this study is still in the pre-clinical stages,” Dr. Markovic-Plese says, “blocking IL-11 could possibly prevent disease development by blocking the early inflammatory response.” If future studies on the neuroprotective effect of IL-11 antibodies continue to show promise, this treatment could be available for MS patients in the near future.

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