Cells continually ingest fluids, solutes, such as proteins, and growth factors via a mechanism called “endocytosis” to ensure their growth and survival — and specialized cells, known as phagocytes, are vital for the ingestion and elimination of invading organisms, such as bacteria and viruses.
Traditional biology teaching states that during endocytosis, the material to be ingested is progressively enclosed by a small portion of the cell or plasma membrane, which first invaginates and then pinches off to form an endocytic vesicle containing the ingested substance or particle. However, despite decades of research, scientists haven’t fully understood how this membrane remodeling process really occurs.
Dr. Sarah Schmitt from the University of Texas Southwestern Medical Center in Dallas has been part of an international team of researchers across the United States, Spain, Russia, and India studying the role of two molecules, dynamin and GTP, in endocytosis.
Their research recently revealed that after molecules known as “coat proteins” pinch the cell’s membrane to form an inward-puckering sac, dynamin wraps itself around the neck of the sac, squeezing it tightly. A jolt of energy from GTP then cuts this neck region, releasing vesicle containing the required contents, and tightly sealing the cell’s outer membrane. GTP has been shown to act by encouraging the membrane to relax, enabling the vesicle to gently pinch off in a relaxed manner.
With a number of genetic defects in endocytosis, being linked to a host of human diseases such as muscular dystrophy, Dr Zimmerberg, from the NIH, hopes that this discovery will forward studies into the understanding of how defects in muscle cell membranes result in the degeneration of muscle tissue in muscular dystrophy.
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