Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0012739 (disseminated intravascular coagulation)
 8,673 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To date, protrusion of pseudopodia has been considered to be primarily responsible for translocation of free-living amoebae and leukocytes of higher organisms. Although there is little question that the pseudopodium plays an important role, little attention has been given to the cortical structures that are responsible for cell-substratum anchorage in amoeboid movement. Here, we report on a new knobby foot-like structure in amoebae of a cellullar slime mold, Dictyostelium discoideum. These feet, each about 1 micron in diameter, appear transiently in multiple units at the base of certain pseudopodia where the amoeba contacts a partially deformable substrate. The feet were discovered, and their spatial and temporal behavior relative to pseudopodial anchorage and invasive locomotion were observed, by examining Dictyostelium amoebae using a DIC video microscope providing an 0.3 micron depth of field. Key evidence for the anchoring role of the knobby feet was obtained by investigating amoebae, flattened in a specially devised observation chamber, and attracted by chemotaxis towards 3',5' cyclic-adenosine monophosphate (cAMP). The cAMP was released by highly localized, pulsed UV-microbeam irradiation of caged cAMP. We show by indirect immunofluorescence that the knobby feet contain a high concentration of filamentous (F-) actin, myoB (a member of Dictyostelium myosin-I family), and alpha-actinin (an actin-binding protein). Interestingly, myoB exhibits a circular disposition around each foot. Neither myosin-II (conventional myosin) nor the 269 kD protein, which has been recently identified as a talin homologue of Dictyostelium [Kreitmeier et al., 1995: J. Cell Biol. 129:179-188], are concentrated at the feet. We propose that the knobby feet provide anchorage to the substratum needed by lamellipodia to exert projectile forces for invading narrow spaces or otherwise for a flattened amoeba to secure itself to the deformable substratum. Some forms of adhesion plaques in higher organisms such as "podosomes" or "invadopodia" may perform functions similar to the knobby feet, but appear to differ in life time, cytoskeletal organization and composition. We have named the knobby foot "eupodium."
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PMID:Amoeboid movement anchored by eupodia, new actin-rich knobby feet in Dictyostelium. 909 56

Previous work has shown that Trypanosoma cruzi extracellular amastigotes as well as metacyclic trypomastigotes infect cultured cells in a highly specific parasite form-cell type interaction. In this work we have investigated the mode of interaction of both forms with HeLa and Vero cells using scanning electron and confocal fluorescence microscopy. We examined the distribution of several host cell components as well as extracellular matrix elements during cell invasion by both T. cruzi infective forms. Scanning electron microscopy showed that membrane expansions formed during the invasion of cells by extracellular amastigotes. These expansions correspond to small cup-like structures in HeLa cells and are comparatively larger "crater"-like in Vero cells. We detected by confocal microscopy actin-rich structures associated with the internalisation of both infective forms of the parasite that correspond to the membrane expansions. Confocal fluorescence microscopy combining DIC images of cells labelled with monoclonal antibodies to phosphotyrosine, cytoskeletal elements, integrins, and extracellular matrix components revealed that some of the components like gelsolin and alpha-actinin accumulate in actin-rich structures formed in the invasion of amastigotes of both cell types. Others, like vinculin and alpha2 integrin may be present in these structures without evident accumulation. And finally, some actin-rich processes may be devoid of components like fibronectin or alphaV integrin. These studies provide evidence that the repertoire of host cell/extracellular matrix components that engage in the invasion process of T. cruzi forms is cell type- and parasite form-dependent.
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PMID:Actin-rich structures formed during the invasion of cultured cells by infective forms of Trypanosoma cruzi. 1066 10