The state of actin assembly regulates actin and vinculin expression by a feedback loop

Bershadsky, Alexander D.; Glück, Ursula; Denisenko, Oleg; Sklyarova, Tatyana; Spector, Ilan; Ben-Ze’ev, Avri

doi:10.1242/jcs.108.3.1183

Cited by 73 publications

(4 citation statements)

References 74 publications

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“…As can be seen in Figure 6B, after nocodazole treatment of HeLa cells, all of the β‐tubulin protein was found in the soluble fraction, whereas the solubility of either DAP‐kinase or actin did not change. In contrast, after treatment of cells with latrunculin A, a microfilament‐disrupting agent (Bershadsky et al ., 1995), a substantial portion of DAP‐kinase was found in the soluble fraction. Here, actin was found almost exclusively in the soluble fraction, whereas the solubility of β‐tubulin was not affected.…”

Section: Resultsmentioning

confidence: 99%

DAP-kinase is a Ca2+/calmodulin-dependent, cytoskeletal-associated protein kinase, with cell death-inducing functions that depend on its catalytic activity

1997

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Kissil et al., 1995). Other laboratories adapted localized to the cytoskeleton, in association with the similar functional selection strategies and candidate genes microfilament system, and mapped a region within that mediate cell death induced by IL-3 deprivation or by the protein which is responsible for binding to the T-cell receptor activation were cloned including Requiem cytoskeleton. Several assays attributed a cell death (Gabig et al., 1994), ALG-2 and ALG-3 (Vito et al., 1996). function to the gene. Ectopic expression of wild-type Our method, called Technical Knock Out (TKO), was DAP-kinase induced the death of target cells, and the based on random inactivation of genes via introduction of killing property depended strictly on the status of the anti-sense cDNA expression libraries, prepared from a intrinsic kinase activity. Conversely, a catalytically mixture of non-treated and IFN-γ-treated cells. The genes inactive mutant that carried a lysine to alanine substituof interest were selected and cloned by virtue of the tion within the kinase domain, displayed dominantdefined phenotypic change-reduced susceptibility to the negative features and protected cells from interferoncytokine-induced cell death-which resulted from their γ-induced cell death. DAP-kinase is therefore a novel inactivation. HeLa cells, transfected with Epstein-Barr cytoskeletal-associated cell death serine/threonine virus (EBV)-based vectors carrying anti-sense cDNA kinase whose activation by Ca 2⍣ /calmodulin may be libraries, were subjected to positive selection of cells that linked to the biochemical mechanism underlying the survived in the continuous presence of IFN-γ. The rescued cytoskeletal alterations that occur during cell death.plasmids that were positively scored in a second round of Keywords: calcium/calmodulin/cytoskeleton/programmed transfection carried six non-overlapping groups of cDNA cell death/serine-threonine kinase fragments. Sequence analysis indicated that five of them corresponded to novel genes: DAPs 1-5 . The sixth gene was identical to a known aspartic protease, i.e. cathepsin D, the participation of which was

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Section: Resultsmentioning

confidence: 99%

DAP-kinase is a Ca2+/calmodulin-dependent, cytoskeletal-associated protein kinase, with cell death-inducing functions that depend on its catalytic activity

1997

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“…However, the quantitative relation of the wavelength to the concentration of cytochalasin was not apparent in this case. The complicated mechansism by which cytochalasin acts to disrupt the actin cytoskeleton creates a nonlinear relationship between drug concentration and the extent of actin polymerization (16)(17)(18). The linear relation of drug concentration to F actin disruption seems to be a unique property of LatA, which is also the only drug whose specificity for actin has been shown genetically (6,7).…”

Section: Explains These Observations In Terms Of the Interplay Betweenmentioning

confidence: 99%

Pearling in cells: A clue to understanding cell shape

Bar‐Ziv

Tlusty

Moses

et al. 1999

Proc. Natl. Acad. Sci. U.S.A.

150

148

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Gradual disruption of the actin cytoskeleton induces a series of structural shape changes in cells leading to a transformation of cylindrical cell extensions into a periodic chain of ''pearls.'' Quantitative measurements of the pearling instability give a square-root behavior for the wavelength as a function of drug concentration. We present a theory that explains these observations in terms of the interplay between rigidity of the submembranous actin shell and tension that is induced by boundary conditions set by adhesion points. The theory allows estimation of the rigidity and thickness of this supporting shell. The same theoretical considerations explain the shape of nonadherent edges in the general case of untreated cells.

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“…We suggest that actin depolymerization might be induced due to palladin depletion by miR96 and miR182; therefore, high amounts of nonpolymerized actin monomers might inhibit actin biosynthesis via a feedback mechanism. It was previously proven that actin depolymerizing agents such as LatA and C2 toxins cause an increase in unassembled actin monomer levels and dramatically reduce the actin biosynthesis via feedback loop mechanism (Bershadsky et al, 1995). We screened putative targets of miR96 and miR182 to identify a possible direct actin regulator and detected ELAVL1 gene encoding HuR protein.…”

Section: Discussionmentioning

confidence: 99%

miR96‐ and miR182‐driven regulation of cytoskeleton results in inhibition of glioblastoma motility

2023

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Glioblastoma multiforme (GBM) is one of the most common forms of brain tumor. As an excessively invasive tumor type, GBM cannot be fully cured due to its invasion ability into healthy brain tissues. Therefore, molecular mechanisms behind GBM migration and invasion need to be deeply investigated for the development of effective GBM treatments. Cellular motility and invasion are strictly associated with the cytoskeleton, especially with actins and tubulins. Palladin, an actin‐binding protein, tightly bundles actins during initial invadopodia and contraction fiber formations, which are essential for cellular motility. Spastin, a microtubule‐binding protein, cuts microtubules into small pieces and acts on invadopodia elongation and cellular trafficking of invadopodia‐associated proteins. Regulation of proteins such as spastin and palladin involved in dynamic reorganization of the cytoskeleton, are rapidly carried out by microRNAs at the posttranscriptional level. Therefore, determining possible regulatory miRNAs of spastin and palladin is critical to elucidate GBM motility. miR96 and miR182 down‐regulate SPAST and PALLD at both transcript and protein levels. Over‐expression of miR96 and miR182 resulted in inhibition of the motility. However, over‐expression of spastin and palladin induced the motility. Spastin and palladin rescue of miR96‐ or miR182‐transfected U251 MG cells resulted in diminished effects of the miRNAs and rescued the motility. Our results demonstrate that miR96 and miR182 over‐expressions inhibit GBM motility by regulating cytoskeleton through spastin and palladin. These findings suggest that miR96 and miR182 should be investigated in more detail for their potential use in GBM therapy.

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The state of actin assembly regulates actin and vinculin expression by a feedback loop

Cited by 73 publications

References 74 publications

DAP-kinase is a Ca2+/calmodulin-dependent, cytoskeletal-associated protein kinase, with cell death-inducing functions that depend on its catalytic activity

DAP-kinase is a Ca2+/calmodulin-dependent, cytoskeletal-associated protein kinase, with cell death-inducing functions that depend on its catalytic activity

Pearling in cells: A clue to understanding cell shape

miR96‐ and miR182‐driven regulation of cytoskeleton results in inhibition of glioblastoma motility

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