This article has been reviewed according to Science X's editorial process and policies. Editors have highlighted the following attributes while ensuring the content's credibility: Every egg cell and sperm cell depends on meiosis, a tightly choreographed process in which chromosomes find their partners, exchange genetic material and then divide. When meiosis goes awry in humans, the consequences can include infertility, miscarriage and birth defects.
A new study from the Stowers Institute for Medical Research, published in Science Advances, shows that the molecular machinery guiding this process is more widely shared across animals than expected, and more flexible. The surprise was that familiar-looking parts were not always doing the same jobs, revealing an unexpected flexibility in how meiosis works across evolution. "That was one of the broader insights from the paper," said Stowers investigator and graduate school president Matt Gibson, Ph.D.
"Proteins and protein complexes may look very much the same, but nevertheless function in different ways." The project was led by Stefanie "Steffi" Williams, Ph.D., a Stowers Graduate School alum who is currently a postdoctoral fellow at the European Molecular Biology Laboratory. At the institute, her work grew from a collaboration between Gibson's lab and the lab of the late R. Scott Hawley, Ph.D., a former Stowers investigator and a pioneer in the field of meiosis.
In this latest study, Williams found that the sea anemone assembles a ladder-like structure called the synaptonemal complex between paired chromosomes, much as humans do. This structure contains eight of the 10 proteins known to make up the synaptonemal complex in humans. But when Williams tested what some of those proteins actually do, the similarities began to break down.
"Despite their essential function, many of the proteins that coordinate meiosis show signatures of rapid evolution, changing much faster than normal housekeeping genes do," said Williams. "So, I was fascinated to find older research showing that cnidarian genomes encode proteins clearly similar to those in humans, and I had to know whether they truly function in the same way." When Williams disabled three of these proteins, the results were unexpected. Mutations in two of them, sycp1 and syce2, caused female sterility.
Males carrying the same mutations remained fertile, and loss of syce2 disrupted the stabilization of paired chromosomes only in females. "When I first sat at the microscope and saw that some components are not required to synapse chromosomes, I thought I must have made a mistake because it didn't make any sense," said Williams. "Finding out that the architectural functions of synaptonemal complex proteins must have changed was totally unexpected." Until now, functional studies of these proteins in animals were largely limited to mice, fruit flies and roundworms.
Extract — continue reading at the source.
