| pubmed-article:8408218 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:8408218 | lifeskim:mentions | umls-concept:C0007634 | lld:lifeskim |
| pubmed-article:8408218 | lifeskim:mentions | umls-concept:C0039259 | lld:lifeskim |
| pubmed-article:8408218 | lifeskim:mentions | umls-concept:C1515654 | lld:lifeskim |
| pubmed-article:8408218 | lifeskim:mentions | umls-concept:C0010839 | lld:lifeskim |
| pubmed-article:8408218 | lifeskim:mentions | umls-concept:C1140999 | lld:lifeskim |
| pubmed-article:8408218 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:8408218 | pubmed:dateCreated | 1993-11-19 | lld:pubmed |
| pubmed-article:8408218 | pubmed:abstractText | We have developed a reconstituted gel-sol and contractile model system that mimics the structure and dynamics found at the ectoplasm/endoplasm interface in the tails of many amoeboid cells. We tested the role of gel-sol transformations of the actin-based cytoskeleton in the regulation of contraction and in the generation of endoplasm from ectoplasm. In a model system with fully phosphorylated myosin II, we demonstrated that either decreasing the actin filament length distribution or decreasing the extent of actin filament cross-linking initiated both a weakening of the gel strength and contraction. However, streaming of the solated gel components occurred only under conditions where the length distribution of actin was decreased, causing a self-destruct process of continued solation and contraction of the gel. These results offer significant support that gel strength plays an important role in the regulation of actin/myosin II-based contractions of the tail cortex in many amoeboid cells as defined by the solation-contraction coupling hypothesis (Taylor, D. L., and M. Fechheimer. 1982. Phil. Trans. Soc. Lond. B. 299:185-197). The competing processes of solation and contraction of the gel would appear to be mutually exclusive. However, it is the temporal-spatial balance of the rate and extent of two stages of solation, coupled to contraction, that can explain the conversion of gelled ectoplasm in the tail to a solated endoplasm within the same small volume, generation of a force for the retraction of tails, maintenance of cell polarity, and creation of a positive hydrostatic pressure to push against the newly formed endoplasm. The mechanism of solation-contraction of cortical cytoplasm may be a general component of the normal movement of a variety of amoeboid cells and may also be a component of other contractile events such as cytokinesis. | lld:pubmed |
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| pubmed-article:8408218 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:8408218 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:8408218 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:8408218 | pubmed:month | Oct | lld:pubmed |
| pubmed-article:8408218 | pubmed:issn | 0021-9525 | lld:pubmed |
| pubmed-article:8408218 | pubmed:author | pubmed-author:TaylorD LDL | lld:pubmed |
| pubmed-article:8408218 | pubmed:author | pubmed-author:JansonL WLW | lld:pubmed |
| pubmed-article:8408218 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:8408218 | pubmed:volume | 123 | lld:pubmed |
| pubmed-article:8408218 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:8408218 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:8408218 | pubmed:pagination | 345-56 | lld:pubmed |
| pubmed-article:8408218 | pubmed:dateRevised | 2011-11-17 | lld:pubmed |
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| pubmed-article:8408218 | pubmed:year | 1993 | lld:pubmed |
| pubmed-article:8408218 | pubmed:articleTitle | In vitro models of tail contraction and cytoplasmic streaming in amoeboid cells. | lld:pubmed |
| pubmed-article:8408218 | pubmed:affiliation | Center for Light Microscope Imaging and Biotechnology, Carnegie Mellon University, Pittsburgh, Pennsylvania 15213. | lld:pubmed |
| pubmed-article:8408218 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:8408218 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:8408218 | pubmed:publicationType | Research Support, U.S. Gov't, Non-P.H.S. | lld:pubmed |
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