Discovery of the mechanism by which cell car engines inhibit its operation to save energy. Molecular motors, in most cell types, work to carry an internal load, as the organelles associated with energy production and transport of nutrients, including the entire cell. We have now discovered how these molecular motors fall into a way of “saving energy”.
Molecular motors:
The cells have small molecular motor for transporting a load such as messenger RNA and organelles within the cell. This transport system is very important, as disruption of motor product of genetic defects leading to fatal diseases in humans.
Molecular motors in nerve cells:
Proteins are the cellular engines play an important role in all eukaryotic cells, but in the case of nerve cells are particularly critical. Proteins synthesized in the body of the cell, as recipients of neurotransmitters need to be transported to the axon. The problems in this transport system may be related to a number of neurological diseases.
Molecular puzzle is solved:
A new study published in Science describes how the engines are folded on themselves, saving energy when not required for their transport services. The molecular puzzle solution provides a new insight into how the proteins regulate the molecular motors that form, and may open new avenues for the treatment of various neurodegenerative diseases like Alzheimer’s and Huntington’s disease.
Saving energy in the neuron cell:
The kinesin motor protein 1 is the main moving a load from the nerve cell body to the axon. A typical kinesin molecule has two tails on one end that attach to the cargo and two globular heads at the other end that go rolling along fibers found inside the cell called microtubules, thus dragging the van load. The movement of the head or motor domain, uses the energy released by breaking ATP, The molecule that stores the energy needed in the functioning of the cell.
When no load, kinesin folds on itself to prevent the ATP waste. Scientists knew that a queue is linked to the two heads to keep the molecule in a state of folding which inhibited normal operation, but the underlying molecular mechanism had remained unclear. It had been suggested some possibilities, but recent findings suggest a single solution.
Inhibition of the motor domain:
The new findings ruled out any proposals that had been done so far on how the tail domain inhibits the motor domain. Not cause a conformational change in the engine, or block surfaces that interact with ATP or microtubule track.
In fact one of the domains of the tail interacts with the head prevents their separation. As the separation of the heads is necessary for the breakdown of the ATP molecule and the consequent generation of energy, this impairment causes the motor to stop generating the “fuel” in the absence of the load.
Other kinesins:
The researchers suggest that other kinesins may be regulated by the same mechanism of self inhibition. Humans have dozens of different motors kinesins that carry a variety of charges, including proteins involved in disease Alzheimer, Huntington and Parkinson.
The kinesins are also involved in the separation of chromosomes during cell division, so these engines can be a target for cancer therapies that attempt to stop the motors that carry chromosomes, which can prevent cancer cells from multiplying.
The research was funded by the Institute of Cancer Research UK, the National Institutes of Health and National Science Foundation in the United States and the Agency for Science, Technology and Research of Singapore.
