Search results
Results from the WOW.Com Content Network
Generally, turgor pressure is caused by the osmotic flow of water and occurs in plants, fungi, and bacteria. The phenomenon is also observed in protists that have cell walls. [3] This system is not seen in animal cells, as the absence of a cell wall would cause the cell to lyse when under too much pressure. [4]
Secondary muscle fibers then form around the primary fibers near the time of innervation. These muscle fibers form from secondary myoblasts and usually develop as fast muscle fibers. Finally, the muscle fibers that form later arise from satellite cells. [3] Two genes significant in muscle fusion are Mef2 and the twist transcription factor.
The negative water potential allows for osmosis to occur in the guard cell, so that water enters, allowing the cell to become turgid. [citation needed] Opening and closure of the stomatal pore is mediated by changes in the turgor pressure of the two guard cells. The turgor pressure of guard cells is controlled by movements of large quantities ...
Two autosomal recessive forms of this disease occur, childhood-onset and adult-onset. The gene for myophosphorylase, PYGM (the muscle-type of the glycogen phosphorylase gene), is located on chromosome 11q13. According to the most recent publications, 95 different mutations have been reported.
Schematic of cell adhesion. Cell adhesion is the process by which cells interact and attach to neighbouring cells through specialised molecules of the cell surface. This process can occur either through direct contact between cell surfaces such as cell junctions or indirect interaction, where cells attach to surrounding extracellular matrix, a gel-like structure containing molecules released ...
Adult skeletal muscle is a possible exception to the rule though their large size makes it difficult to be certain of this. An argument used against skeletal muscle gap junctions is that if they were present gap junctions may propagate contractions in an arbitrary way through cells making up the muscle.
The inability to break down glycogen within the lysosomes of cells leads to progressive muscle weakness throughout the body and affects various body tissues, particularly in the heart, skeletal muscles, liver and the nervous system. GSD-II and Danon disease are the only glycogen storage diseases characterised by a defect in lysosomal metabolism.
[9] [23] In muscles, the inability of cells to efficiently breakdown glycogen due to the severe reduction or absence of branching can lead to muscle weakness and atrophy. [9] At least three mutations in the GBE1 gene have been found to cause another disease called adult polyglucosan body disease (APBD).