Ctsl pursues Cux1 inside the nucleus and cleaves it, creating a smaller protein with different transcriptional properties than the original one. During the cell cycle, Ctsl can target a transcription factor – a protein that binds specific DNA sequences - called Cut-like 1 (Cux1) that plays a role in gene expression. The mammalian version of Cp1 is a protein known to be associated with cancer progression and other diseases called lysosomal protein capthesin-L (Ctsl). "We investigated whether it was possible that Cp1, during metamorphosis, shuttles from the cytoplasm into the nucleus to cleave a transcription factor required for dendrite development, and makes it a new transcription factor for regeneration," Kuo said. Kuo's team demonstrated that without Cp1, drosophila sensory dendrites cannot regenerate after pruning.Įxisting literature also pointed Kuo's team to a parallel between the drosophila nervous system and mammals. The dendrite design and architecture was, in fact, different in the adult stage.Ī test carried out by former graduate student Gray Lyons revealed Cysteine proteinase-1 (Cp1) is responsible for regulating the regeneration of neuron dendrites and innervating the adult sensory field. To find out how the drosophila sensory neurons accomplish this change, Kuo's team tagged abdominal sensory neurons with green fluorescent protein (GFP) and followed them through metamorphosis to see if their dendrite branching changed. The regeneration process, which is controlled by the hormone ecdysone, is much like pruning a tree in spring to make room for new growth, Kuo said. The remaining sensory neurons sever their dendrites and grow a completely different set. During this transition, Drosophila lose the neurons they won't need for adult life. The answer lies in the insect's metamorphosis from larvae to adult. Endowment, will appear online in the Feb. Sloan Foundation and the George & Jean Brumley, Jr. His team set out to find the genetic mechanism that makes it possible. Until now, researchers haven’t understood how drosophila sensory neurons are able to create two separate dendrite branching patterns that successfully serve different kinds of sensory environments, said Kuo, who is also a faculty member with the Duke Institute for Brain Sciences (DIBS). As an adult with bristle-covered skin however, the nervous system must be wired for flying, finding mates and laying eggs. In the larval (or worm) state, the fly's nervous system is attuned to what the smooth-skinned worm needs: finding food, locomotion and avoiding attack. While prompting such regrowth in the human brain isn't currently possible, dendrite regeneration and arborization - the branching out of dendrites from the body of the neuron - are a necessary part of the fruit fly Drosophila's life cycle. "Neurons don't multiply, so when they're injured, there's a loss of function. Brumley assistant professor of cell biology, neurobiology and pediatrics. "One of the major problems with the nervous system is that it doesn't regenerate very well after injury," said Chay Kuo, M.D., Ph.D., the George W. ![]() But if a neuron is injured or malformed, they frequently don't have the proper dendrites needed to be functional. Under normal circumstances, neural communication is easy, much like neighbors talking over a fence. Incorrect dendrite development or injury has been linked to neurodevelopmental or psychiatric diseases in humans, such as autism, schizophrenia and fragile X syndrome. ![]() Known as dendrites, these thin structures that resemble tree branches are responsible for receiving electrical impulses that flash throughout the body. This protein directs both the early development and regrowth of the tiny branches that relay information from neuron to neuron. A protein that controls the metamorphosis of the common fruit fly could someday play a role in reversing brain injuries, said Duke University researchers.
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