Researchers Find 'Fusion' Protein

Working with fruit flies, scientists at Johns Hopkins have discovered a protein required for two neighboring cells to fuse and become one "super cell."

Most cells enjoy their singular existence, but the strength and flexibility of muscles relies on hundreds or even thousands of super cells that make large-scale motion smooth and coordinated, such as flexion of a bicep.

The newly discovered protein, dubbed Solitary, coordinates the movement of tiny molecular delivery trucks to a cell's surface. Cells that lack Solitary stay, well, solitary. "They refuse to fuse," says Hopkins assistant professor of molecular biology and genetics Elizabeth Chen, Ph.D., whose report on the work is online this week in Developmental Cell.

Chen and her team studied fruit fly embryo muscles to find the molecular signals that tell two neighboring cells to join as one, plucking out for further study those embryos containing cells that refused to fuse.

They then compared the genetic sequences from healthy embryos with sequences from defective embryos to locate differences and identify the genes responsible for unfused muscle cells. In the process, they identified Solitary.

Chen's team next made a tool to see the Solitary protein, enabling them to track its localization under a fluorescent microscope. At each future fusion point between cells that they examined in the fly muscles, they saw concentrations of glowing clumps of Solitary protein.

"As we uncover more of the players in cell fusion, we get closer to manipulating fusion for our benefit," Chen adds. Muscular dystrophy, for example, might be treated by injecting into patients healthy muscle cells that are designed to fuse efficiently with the diseased muscles, saving the diseased cells from deteriorating.

They also discovered that Solitary protein is attached to the cell's skeleton. "It was so bizarre to see Solitary - something meant to regulate the cell's internal structure - to be involved in the external events of cell fusion," says Chen.

But in addition to structural support, the cell's "skeleton" provides an internal railway of sorts, along which other proteins and molecules can move. Indeed, the researchers saw that while normal cells were able to shuttle tiny storage compartments within the cell - presumably holding important molecular tools needed for cell fusion - to the fusion site, these storage compartments were scattered haphazardly, seemingly lost in the cellular wilderness, in cells lacking Solitary.

When two neighboring cells fuse, they need to break down the barrier between them, explains Chen. It turns out that the Solitary protein marks where that break is happening and subsequently tells the cell where to build its skeleton railway. "In this role, Solitary acts not like the delivery truck, but more like a construction site foreman," says Chen. "It's told where the cell barrier needs to be broken, then directs the building of a delivery road so that the molecular supplies can be brought to the fusion site."

Source: Johns Hopkins Medical Institutions

Related stories:

Gene that causes childhood cancer neuroblastoma is found
Scientists have discovered gene mutations that are the main cause of the inherited version of the childhood cancer neuroblastoma. In addition, the researchers found that the same mutations play a significant role in high-risk forms of non-inherited neuroblastoma, the more common form of the disease.
Scientists nail childhood nerve cancer gene
Researchers have identified the hereditary gene mutations behind a deadly form of childhood cancer, opening the way to genetic tests in high-risk families, according to study released Sunday.
Researchers Capture Images that Illuminate One of Cell's Mysteries
(PhysOrg.com) -- Within human cells, tiny membrane-bound compartments called vesicles shepherd biomolecules from place to place.
Researchers Discover Remnant of an Ancient 'RNA World'
(PhysOrg.com) -- Some bacterial cells can swim, morph into new forms and even become dangerously virulent - all without initial involvement of DNA. Yale University researchers describe Friday in the journal Science how bacteria accomplish this amazing feat - and in doing so provide a glimpse of what the earliest forms of life on Earth may have looked like.
Not the protein, but its location in the cell, determines the onset of leukemia
Scientists are still searching for the cause of many forms of Leukemia, including T-cell acute lymphoblastic leukemia. VIB researchers connected to the Katholieke Universiteit Leuven have discovered that the carcinogenic property of the fusion protein NUP214-ABL1 largely depends on its location in the cell. Casting new light on the biological processes behind T-ALL, this finding is important in the search for new targeted therapies that are less toxic than chemotherapy.
Researchers identify tumor suppressor that manages cellular cleaning and recycling proceses
Researchers at the University of Southern California (USC) have identified a specific tumor suppressor that manages membrane traffic routes for cellular cleaning and recycling.
Protein linked to Alzheimer's disease also has role in HIV progression
The apolipoprotein (apo) E4 isoform has been implicated in neurodegeneration in Alzheimer's disease, cardiovascular disease, and stroke. Now, investigators at the Gladstone Institutes, the University of California, San Francisco, the University of Texas Health Science Center at San Antonio, and the Infectious Disease Clinical Research Program, Uniformed Services University, Bethesda, Maryland have shown that this troubling protein is a risk factor for AIDS progression rates and promotes entry of HIV into cells. The study was published in today's issue of the Proceedings of the National Academy of Sciences USA (PNAS).
Outing the outliers: Strategy matches oncogene with subtype of prostate cancer
A new study reveals a previously unidentified candidate oncogene that appears to play a significant role in a subset of prostate cancers. The research, published by Cell Press in the June issue of the journal Cancer Cell, describes a new strategy that can be used to find "outlier" genes in cancer subtypes that are not well understood.

News discussion:

General Science news