For decades, this one sat in the dark. Scientists knew a small nutrient-like compound mattered for human health, but they did not know how it got into our cells.
Now an international team of researchers, led in part by scientists at the University of Florida and Trinity College Dublin, says it has solved that puzzle.
In a study published this week in the Proceedings of the National Academy of Sciences, the researchers identified the gene responsible for transporting queuosine into human cells. Queuosine, pronounced “cue-o-scene,” is a vitamin-like compound that the body cannot produce on its own. It comes instead from certain foods and from bacteria living in the gut.
The finding could eventually support the development of new treatments built around queuosine’s roles in memory, learning and cancer suppression, according to the researchers.
“For over 30 years, scientists have suspected that there had to be a transporter for this nutrient, but no one could find it,” said Valérie de Crécy-Lagard, a UF/IFAS microbiology and cell science distinguished professor and department associate chair, and one of the study’s principal investigators.
“We’ve been hunting for it for a long time. This discovery opens up a whole new chapter in understanding how the microbiome and our diet can influence the translation of our genes.”
Queuosine was first identified in the 1970s, but remained largely overlooked for decades despite its importance, the researchers said.
The compound plays a key role in how the body builds proteins. It alters transfer RNA, the molecules that help cells interpret DNA and produce proteins correctly.
“It’s like a nutrient that fine-tunes how your body reads your genes,” de Crécy-Lagard said. “The idea that this small compound, which people have barely heard of, plays such an important role, is fascinating.”
For years, scientists did not know how queuosine entered cells. The new study identifies the gene SLC35F2 as the missing transporter.
The researchers said that fills a major gap in the biology of the compound and gives future studies a starting point.
SLC35F2 had already been studied for a different reason. Scientists knew it played a role in allowing viruses and some cancer drugs to enter cells. But its normal function in healthy biology had remained unclear until now, de Crécy-Lagard said.
“We have known for a long time that queuosine influences critical processes like brain health, metabolic regulation, cancer and even responses to stress, but until now we haven’t known how it is salvaged from the gut and distributed to the billions of human cells that take it in,” said Vincent Kelly, professor in Trinity College Dublin’s School of Biochemistry and Immunology, and joint senior author of the article.
The study was supported by several national health organisations, including the National Institutes of Health, Research Ireland, formerly Science Foundation Ireland, and Health and Social Care in Northern Ireland.
The project brought together scientists from the University of Florida, San Diego State University, the Ohio State University, and institutions across Ireland and Northern Ireland.
The researchers said that broad effort was a big part of why the work succeeded.
“We don’t think we could have cracked it without the full team,” de Crécy-Lagard said. “It’s a perfect example of what international collaboration can achieve.”
