Gap Junction Structure
Connexin proteins make up gap junctions in the cells of vertebrates. (Gap junctions in invertebrate cells are made up of innexin proteins, which are unrelated to connexin proteins but serve a similar purpose.) A connexon is made up of six connexin groups, and two connexons combined make a channel through which molecules can move. Pannexin proteins make up additional channels in gap junctions. Pannexins were first believed to only create channels within a cell, not across cells, hence they are still relatively poorly understood. In what is referred to as a gap junction plaque, hundreds of channels are discovered together at the location of a gap junction. A mass of proteins makes up a plaque
Function
Electrically excitable cells, like neurons, the heart, and smooth muscle, depend on the ability of nearby cells to transfer ions through low-resistance routes to function. The characteristics of gap junctions (electrical synapses) for electrical transmission between neighbouring cells led to their discovery in the heart and nerve. When cells are connected by gap junctions, synaptic transmission is accelerated and groups of cells can be synchronised for coordinated electrical and mechanical output.
Almost all of the cells in solid tissues, aside from those that are electrically excitable, are connected by gap junctions. GJIC’s primary job is to distribute metabolic demands among cell groups, which act as a buffer against spatial gradients of nutrients or signalling chemicals. For instance, it has been demonstrated that the targeted deletion of Cx32 in mice causes a lack of sympathetic reactivity, which impairs the mobilisation of glucose from glycogen reserves. Only a portion of the hepatocytes can be directly stimulated by postganglionic sympathetic axons because they terminate at the borders of the liver lobules. It is assumed that second messengers diffuse through gap junctions to indirectly excite the remaining portion of the lobule. To prevent the loss of a vital metabolic enzyme or ion channel in one cell, gap junctions may also act as suppressors of somatic cell mutations. For instance, hypoxanthine phosphoribosyltransferase (HGPRTase), a crucial enzyme in the nucleotide salvage pathway, is compromised, which leads to Lesch-Nyhan syndrome. Impaired HGPRTase causes a rise in phosphoribosyl pyrophosphate levels, a notable acceleration of purine biosynthesis, and an excess generation of urate. Metabolic collaboration, or gap junction creation with normal cells, can metabolically restore mutant fibroblasts from Lesch-Nyhan syndrome patients in cell culture. Furthermore, the absence of symptoms in heterozygous female Lesch-Nyhan carriers is probably explained by metabolic cooperation. Given that HGPRTase resides on the X chromosome, a mosaic of mutant and healthy cells is produced when the X chromosome is randomly inactivated. Individuals are thus asymptomatic as a result of nearby nonmutant cells’ metabolic rescue of mutant cells.
Gap Junction
The fundamental structural and operational unit of all living things is the cell. Each cell has a cytoplasm that is surrounded by a membrane and is home to a variety of biomolecules, including proteins and nucleic acids.
Cells can develop specialised functions and perform a variety of tasks within the cell, including protein synthesis, DNA repair, replication, and motility. Within the cell, cells can specialise and move around. Due to their small size, the majority of cells are measured in micrometres.
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