美国约翰霍普金斯 (Johns Hopkins)的科学家，透过了果蝇的研究系统，找到了一个特殊的蛋白质，可以将两个细胞黏合在一起，形成所谓融合细胞的超级细胞 (Super Cell) 科学家表示，细胞虽然都是一个个进行分裂复制的行为，但是要执行特定的生理功能的时候，往往得群聚在一起，像是肌肉组织进行收缩的活动时，若仅有少数的细胞，就没有办法达到一定的强度，因此细胞间彼此接触融合共同运作的模式，几乎是成功生理活动的一个关键。
 这次研究人员利用果蝇的胚胎发育系统，成功的找到了一个称为 Solitary的蛋白质，在功能上不但是协调输送小分子到细胞表面的输送介质，还是细胞间彼此黏合的主角，因为细胞里的 Solitary功能异常时，相同的细胞在发育的过程，并不会靠拢，因此往往失去原先该有的功能。
科学家怀疑一些肌无力或是肌肉细胞病变的遗传疾病，很可能也是这类基因的功能出现了异常所导致，因此未来透过大规模的定序比对，将有机会因此 Solitary蛋白质的发现，找到新的方法可以治疗目前无解的肌肉病变相关疾病。
英文原文：
'Fusion' Protein Found by Johns Hopkins Researchers
| 04/11/07 -- 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 |
Developmental Cell, Vol 12, 571-586, 09 April 2007
Article
A Critical Function for the Actin Cytoskeleton in Targeted Exocytosis of Prefusion Vesicles during Myoblast Fusion
Sangjoon Kim,1,2 Khurts Shilagardi,1,2 Shiliang Zhang,1,2 Sabrina N. Hong,1 Kristin L. Sens,1 Jinyan Bo,1 Guillermo A. Gonzalez,1 and Elizabeth H. Chen1,
1 Department of Molecular Biology and Genetics, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
Corresponding author
Elizabeth H. Chen
echen@jhmi.edu
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