Posts tagged organelles
Articles and news from the latest research reports.
Study of the machinery of cells reveals clues to neurological disorder
Investigation by researchers from the University of Exeter and ETH Zurich has shed new light on a protein which is linked to a common neurological disorder called Charcot-Marie-Tooth disease.
Peroxisomes (green) and mitochondria (red) in a mammalian cell. The nucleus (blue) contains the cellular DNA.
The team has discovered that a protein previously identified on mitochondria - the energy factories of the cell - is also found on the fat-metabolising organelles peroxisomes, suggesting a closer link between the two organelles.
Charcot-Marie-Tooth disease is currently incurable and affects around one in every 2,500 people in the UK, meaning that it is one of the most common inherited neurological disorders, thus understanding the molecular basis of the disease is of great importance. Symptoms can range from tremors and loss of touch sensation in the feet and legs to difficulties with breathing, swallowing, speaking, hearing and vision.
The research published online in EMBO Reports combines work from University of Exeter Biosciences researcher Dr Michael Schrader and PhD student Sofia Guimaraes. The major finding of the study is that the protein GDAP1, originally thought to only be involved in fragmentation of mitochondria, also contributes to the regulation of peroxisome number through their division.
Peroxisomes are small organelles occurring in nearly all cells, from yeast to crop plants to humans, and are essential for cell viability due to their important role in the metabolism of fatty acids and reactive oxygen species. Peroxisomes are also of particular interest as they play a key role in ageing.
This current study shows that the division of both mitochondria and peroxisomes follows a similar mechanism, although many of the disease-causing mutations occur in a region of the gene that is more critical for mitochondrial than peroxisomal division.
Dr Michael Schrader said of this project: “This study supports our hypothesis of a closer connection between mitochondria and peroxisomes. We have identified several membrane proteins, which are shared by both organelles, particularly key components of the division machinery, meaning there must be coordinated biogenesis and cross-talk.”
As numerous diseases have been linked to problems in the mitochondria, Dr Schrader proposes that this connection could have far-reaching medical implications.
This work contributes to the research being addressed through the prestigious Marie Curie Initial Training Network PERFUME programme (PERoxisome, FUnction, and MEtabolism), recently awarded to Michael Schrader along with several other top European research groups which focus on peroxisome biology.
(Source: exeter.ac.uk)
Tiny worm sheds light on giant mystery about neurons
Scientists have identified a gene that keeps our nerve fibers from clogging up. Researchers in Ken Miller’s laboratory at the Oklahoma Medical Research Foundation (OMRF) found that the unc-16 gene of the roundworm Caenorhabditis elegans encodes a gatekeeper that restricts flow of cellular organelles from the cell body to the axon, a long, narrow extension that neurons use for signaling. Organelles clogging the axon could interfere with neuronal signaling or cause the axon to degenerate, leading to neurodegenerative disorders. This research, published in the May 2013 Genetics Society of America’s journal GENETICS, adds an unexpected twist to our understanding of trafficking within neurons.
Proteins equivalent to UNC-16 are present in the neurons of all animals, including humans And are known to interact with proteins associated with neurodegenerative disorders in humans (Hereditary Spastic Paraplegia) and mice (Legs at Odd Angles). However, the underlying cause of these disorders is not well understood.
"Our UNC-16 study provides the first insights into a previously unrecognized trafficking system that protects axons from invasion by organelles from the cell soma," Dr. Miller said. "A breakdown in this gatekeeper may be the underlying cause of this group of disorders," he added.
The use of the model organism C. elegans, a tiny, translucent roundworm with only 300 neurons, enabled the discovery because the researchers were able to apply complex genetic techniques and imaging methods in living organisms, which would be impossible in larger animals. Dr. Miller’s team tagged organelles with fluorescent proteins and then used time-lapse imaging to follow the movements of the organelles. In normal axons, organelles exited the cell body and entered the initial segment of the axon, but did not move beyond that. In axons of unc-16 mutants, the organelles hitched a ride on tiny motors that carried them deep into the axon, where they accumulated.
Dr. Miller acknowledges there are still a lot of unanswered questions. His lab is currently investigating how UNC-16 performs its crucial gatekeeper function by looking for other mutant worms with similar phenotypes. A Commentary on the article, also published in this issue of GENETICS, calls the work “provocative”, and highlights several important questions prompted by this pioneering study.
"This research once again shows how studies of simple model organisms can bring insight into complex neurodegenerative diseases in humans," said Mark Johnston, Editor-in-Chief of the journal GENETICS. “This kind of basic research is necessary if we are to understand diseases that can’t easily be studied in more complex animals.”
(Source: eurekalert.org)
!['Zombie' replica cells may outperform live ones as catalysts and conductors
"Zombie" mammalian cells that may function better after they die have been created by researchers at Sandia National Laboratories and the University of New Mexico (UNM).
The simple technique coats a cell with a silica solution to form a near-perfect replica of its structure. The process may simplify a wide variety of commercial fabrication processes from the nano- to macroscale.
The work, reported in the Proceedings of the National Academy of Sciences (PNAS), uses the nanoscopic organelles and other tiny components of mammalian cells as fragile templates on which to deposit silica. The researchers then heat the cell to burn off its protein. The resultant hardened silica structures are faithful to the exterior and interior features of the formerly living cell, can survive greater pressures and temperatures than flesh ever could, and can perform some functions better than when they were alive, said lead researcher Bryan Kaehr, a Sandia materials scientist.
"It’s very challenging for researchers to build structures at the nanometer scale," said Kaehr. "We can make particles and wires, but 3-D arbitrary structures haven’t been achieved yet. With this technique, we don’t need to build those structures—nature does it for us. We only need to find cells that possess the machinery we want and copy it using our technique. And, using chemistry or surface patterning, we can program a group of cells to form whatever shape seems desirable."
UNM professor and Sandia Fellow Jeff Brinker added, “The process faithfully replicates features from the nanoscale to macroscale in a robust, three-dimensionally stable form that resists shrinkage even upon heating to over 500 degrees Centigrade [932 degrees Fahrenheit]. The refractoriness of these delicate structures is amazing.”](http://41.media.tumblr.com/ab71a5f63d10d4f295ad6ced72ef3eb5/tumblr_mi0kfyBhql1rog5d1o1_500.jpg)
'Zombie' replica cells may outperform live ones as catalysts and conductors
"Zombie" mammalian cells that may function better after they die have been created by researchers at Sandia National Laboratories and the University of New Mexico (UNM).
The simple technique coats a cell with a silica solution to form a near-perfect replica of its structure. The process may simplify a wide variety of commercial fabrication processes from the nano- to macroscale.
The work, reported in the Proceedings of the National Academy of Sciences (PNAS), uses the nanoscopic organelles and other tiny components of mammalian cells as fragile templates on which to deposit silica. The researchers then heat the cell to burn off its protein. The resultant hardened silica structures are faithful to the exterior and interior features of the formerly living cell, can survive greater pressures and temperatures than flesh ever could, and can perform some functions better than when they were alive, said lead researcher Bryan Kaehr, a Sandia materials scientist.
"It’s very challenging for researchers to build structures at the nanometer scale," said Kaehr. "We can make particles and wires, but 3-D arbitrary structures haven’t been achieved yet. With this technique, we don’t need to build those structures—nature does it for us. We only need to find cells that possess the machinery we want and copy it using our technique. And, using chemistry or surface patterning, we can program a group of cells to form whatever shape seems desirable."
UNM professor and Sandia Fellow Jeff Brinker added, “The process faithfully replicates features from the nanoscale to macroscale in a robust, three-dimensionally stable form that resists shrinkage even upon heating to over 500 degrees Centigrade [932 degrees Fahrenheit]. The refractoriness of these delicate structures is amazing.”