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News / 11.16.18

Research Roundup: November 16, 2018

Erik Jacobs
Credit : Erik Jacobs
By Broad Communications

Serine's mitochondrial entry point, science's better mosquito genome, and malaria's new drug resistance route.

Welcome to the November 16, 2018 installment of Research Roundup, a recurring snapshot of recent studies published by scientists at the Broad Institute and their collaborators.

Study shows serine’s secret sender

The generation of one-carbon units is necessary for synthesizing many critical metabolites in the body, but scientists have wondered about a key step in this process: the entry of serine into the mitochondria. Reporting in Science, associate member David Sabatini, Nora Kory (Whitehead Institute), and colleagues describe their CRISPR-based screen in human cells, which pointed to sideroflexin 1 (SFXN1). They performed functional studies of SFXN1, which revealed that the protein in fact acts as a mitochondrial serine transporter in one-carbon metabolism.

Accelerating mosquito science with genomics

Each year, more than 400 million people contract mosquito-borne illnesses such as dengue, yellow fever, Zika, and chikungunya. Though they have long known that female Aedes aegypti mosquitoes transfer these disease-causing pathogens, researchers still lacked a complete understanding of its genome. An international team of researchers, including Seth Redmond and associate member Daniel Neafsey in the Infectious Disease and Microbiome Program (IDMP), has combined advanced genomic technologies to provide a new, high-resolution blueprint of the Ae. aegypti genome. With a renewed view of the mosquito genome, researchers should be able to gather further biological insights and develop improved strategies to control disease vectors. Read more in Nature and a Rockefeller University press release.

Exploring artemisinin resistance

The spread of the malaria parasite (Plasmodium falciparum) with reduced susceptibility to artemisinin presents a threat to global disease control. Most failures of artemisinin treatment are attributed to mutations in the parasite’s pfkelch13 gene locus, acting through an unclear mechanism. A team led by IDMP senior associate member Dyann Wirth and colleagues now reports a new route that the parasite can take to artemisinin resistance, based on mutations in the gene pfcoronin. The discovery of a second possible gene involved in artemisinin resistance may yield new insights into the molecular mechanisms at play. Learn more in PNAS.

To learn more about research conducted at the Broad, visit broadinstitute.org/publications, and keep an eye on broadinstitute.org/news.

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Infectious Disease and Microbiome Program