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Gap Junctions.docx

Gap Junctions.docx

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Published by: Denise Janelle Enriquez Geraldizo on Aug 05, 2013
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By definition, gap junctions are plasma membrane spatial microdomains constructed of assemblies of channel proteins called connexins in vertebrates

and innexins in invertebrates. It attaches directly to the cytoplasm of two cells, to which allows various molecules and ions to pass freely between the cells. Protienaceous tubes that connect adjacent cells. These tubes allow material to pass from one cell to the next without having to pass through the plasma membranes of the cells. Dissolved substances such as ions or glucose can pass through the gap junctions. Large organelles such as mitochondria connot pass. Gap junctions allow adjacent cells in animal tissues to communicate with one another. Gap junctions act as a tunnel bridging the plasma membranes of two neighboring cells, connecting their cytoplasms and allowing small molecules or ions to flow between them. A good example are the gap junctions found in the mycardium (heart muscles).Electrical impulses are propagated by the flow of ions. In chemical synapses, there is delay as the electrical impulse (action potential) arriving at the terminal buds of the presynaptic axon must be converted into a cellular response, where synaptic vesicles are made to undergo exocytosis, their contents must diffuse across the synapse, must bind to receptors on the postsynaptic neuron, and bring the postsynaptic neuron to threshhold - all before the impulse travels from one neuron to the next. Heart muscle cells have electrical synapses. The flow of ions does not have to cease for the intervening chemical process to occur. Instead, the flow of ions travels through the gap junctions 'instantly', allowing all the muscle cells of, say, the left ventricle, to contract at the same time, thus producing a coordinated pumping force. Compared to the reduction of excitability, critical gap junction disconnects the conduction velocities to a larger extend and is safer for conduction to occur. In uniformly structured tissue, gap junctional uncoupling is accompanied by a parallel decrease in conduction velocity. Nevertheless, partial uncoupling paradoxically increases conduction like tissue expansion which has the capacity to remove unidirectional conduction blocks. The role of gap junctions for the velocity and the safety of impulse propagation in cardiac tissue is very essential. The specific subcellular distribution of gap junctions together with the tight packaging of the rod-shaped cardiomyocytes underlies anisotropic conduction, which is continuous at the macroscopic scale in physiologic conditions. But, the three-dimensional network of cells into linear single cell chains, gap junctions can be shown to limit axial current flow and to induce ‘saltatory’ conduction at unchanged overall conduction velocities when breaking down. These discontinuities disappear due to lateral averaging of depolarizing current flow at the activation wave front in two and three dimensional tissues. In addition, gap junctions are particularly important in cardiac muscle: the signal to contract is passed efficiently through gap junctions, allowing the heart muscle cells to contract in tandem. It is expressed in virtually all tissues of the body, with the exception of mobile cell types such as sperm or erythrocytes. Several human genetic disorders are associated with mutations in gap junction genes. On the other hand, connexin or also known as gap junction proteins are somehow related transmembrane proteins that assemble to form vertebrate gap junctions. Each of the gap junction is composed of two hemichannels, or connexons, which are themselves each constructed out of six connexin molecules. For many physiological processes, such as the coordinated depolarization of cardiac muscle, proper embryonic development, and the conducted response in microvasculature, gap junction is very important. For this statement, mutations in proteins-encoding genes can lead to functional and or developmental abnormalities. Cell adhesion proteins may contribute to the docking and assembling process. The connexin subunit is a four-transmembrane spanning protein, harboring two extracellular, one cytoplasmic loop and one cytoplasmatic N- as well as C-terminal region. Six connexin (Cx) subunits can form a hemichannel in the plasma membrane that can berth to another hemi-channel in the plasma membrane of

Innexins form another family of gap junctional proteins that are only expressed in invertebrates (D. elegans) and do not show any sequence similarity to connexins.The human connexin 43 genes. and neurodegeneration. in cell growth control and cell communication and signaling. Researchers found mutations in the GJA1 gene in all 17 families with oculodentodigital dysplasia that they screened. connexin can cause human disorders like the Connexin 26 that causes hear loss. which normally instructs a protein. Structures and functions of Connexin must be further being studied to prevent the mutation of connexins and to cure this human disorders for those who already got the mutated connexins like the Connexin 26 and Connexin 43. This is a complex genetic disorder that leads to flawed copies of the gap junction beta 2 (GJB2) genes. Connexin 26 (CX26). Recently. . Another disorder caused by connexin is the connexin 43. A substantial portion of people with nonsyndromic hearing loss have Connexin 26 disorder. spastic paraplegia. and cardiac abnormalities are observed in rare instances. To sum up. connexins are helpful in Cardiac action potentials. These mutations may cause misassembly of channels or alter channel conduction properties. genes that show some sequence identity to innexins were also discovered in the genome of higher vertebrates therefore designated as pannexins. Syndactyly type III and conductive deafness can occur in some cases. Abnormalities can lower one’s self-esteem and difficulty in living and surviving in this world and can cause inequalities in the community. Sixteen different missense mutations and one codon duplication were detected. Expression patterns and phenotypic features of gja1 animal mutants. melanogaster or C. but mutation in this connexins can cause human disorders like hear loss and cause Skin disease and maybe more critical disorders in the future. and dental) and limb dysmorphisms. Advances in genetics have enabled scientists to identify genes that cause hearing loss. Within both extracellular loops. or GJA1. reported elsewhere. are compatible with the pleiotropic clinical presentation of oculodentodigital dysplasia. This autosomal dominant syndrome presents with craniofacial (ocular. Sometimes. nasal. the order of three cysteine residues is highly conserved (except for Cx31): first loop: [C–X6–C–X3– C] and second loop [C–X5–C–X5–C].an adjacent cell. is located at human chromosome 6q22-q23 within the candidate region for the oculodentodigital dysplasia locus. in order to assemble a complete gap junctional channel. Opposing cysteines in both loops were suggested to form disulfidebridges stabilizing the loops during the docking of two connexons.

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