Mitochondria are associated with microtubules and not with intermediate filaments in cultured fibroblasts.

Ball, Eric H.; Singer, S. J.

doi:10.1073/pnas.79.1.123

Cited by 205 publications

(91 citation statements)

References 45 publications

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“…The remarkable organdies in fibroblasts are mitochondria which can be easily revealed with rhodamine-123 vital staining. It has been shown that mitochondria coaligned with microtubules in fibroblasts and their distribution depended on microtubule network (Ball and Singer, 1982). Moreover, kinesin has been reported to associate with isolated mitochondria and could be revealed in patches on the mitochondrial surface by immunostaining (Leopold et al, 1992).…”

Section: Discussionmentioning

confidence: 99%

“…To check whether this antibody affected the intracellular transport of membranous organelles in fibroblasts as well, we analyzed the distribution of mitochondria in the cells in- jected with the antibody. It is well known that mitochondria coalign with microtubules in fibroblasts and their distribution was found to depend on the integrity of the cytoplasmic microtubule network (Ball and Singer, 1982). Fig.…”

Section: Antibody L I D Interferes With Mitochondria Distribution In mentioning

confidence: 99%

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Microtubule-dependent control of cell shape and pseudopodial activity is inhibited by the antibody to kinesin motor domain.

Rodionov

Gyoeva

Tanaka

et al. 1993

The Journal of Cell Biology

149

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Abstract. One of the major functions of cytoplasmic microtubules is their involvement in maintenance of asymmetric cell shape. Microtubules were considered to perform this function working as rigid structural elements. At the same time, microtubules play a critical role in intracellular organelle transport, and this fact raises the possibility that the involvement of microtubules in maintenance of cell shape may be mediated by directed transport of certain cellular components to a limited area of the cell surface (e.g., to the leading edge) rather than by their functioning as a mechanical support. To test this hypothesis we microinjected cultured human fibroblasts with the antibody (called HD antibody) raised against kinesin motor domain highly conserved among the different members of kinesin superfamily. As was shown before, this antibody inhibits kinesin-dependent microtubule gliding in vitro and interferes with a number of microtubule-dependent transport processes in living cells. Preimmune IgG fraction was used for control experiments. Injections of fibroblasts with HD antibody but not with preimmune IgG significantly reduced their asymmetry, resulting in loss of long processes and elongated cell shape. In addition, antibody injection suppressed pseudopodial activity at the leading edge of fibroblasts moving into an experimentally made wound. Analysis of membrane organelle distribution showed that kinesin antibody induced clustering of mitochondria in perinuclear region and their withdrawal from peripheral parts of the cytoplasm. HD antibody does not affect either density or distribution of cytoplasmic microtubules. The results of our experiments show that many changes of phenotype induced in cells by microtubule-depolymerizing agents can be mimicked by the inhibition of motor proteins, and therefore microtubule functions in maintaining of the cell shape and polarity are mediated by motor proteins rather than by being provided by rigidity of tubulin polymer itself.

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Section: Discussionmentioning

confidence: 99%

Section: Antibody L I D Interferes With Mitochondria Distribution In mentioning

confidence: 99%

Microtubule-dependent control of cell shape and pseudopodial activity is inhibited by the antibody to kinesin motor domain.

Rodionov

Gyoeva

Tanaka

et al. 1993

The Journal of Cell Biology

149

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“…Mitochondria utilize the contractile force of the microtubules for their intracellular motility, but its significance and regulation remain elusive [45]. It is also currently unknown whether such movements have any impact in innate immunity.…”

Section: Mitochondrial Motility Is Essential For Nsd Functionmentioning

confidence: 99%

“…Second, in live cells, the mitochondria undergo dynamic changes in length and shape through fusion and fission [43,44]. Lastly, the mitochondria are also highly motile and swim around the cytosol through the use of the contractile microtubule network [45,46]. In the following sections, we IFN induction and IFN response were quantified by the appropriate Luc reporter assays, and RSV growth was measured by plaque assay in Hep-2 cells as previously described [28,38].…”

Section: Ramansu Goswami Et Al 1031mentioning

confidence: 99%

Viral degradasome hijacks mitochondria to suppress innate immunity

et al. 2013

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The balance between the innate immunity of the host and the ability of a pathogen to evade it strongly influences pathogenesis and virulence. The two nonstructural (NS) proteins, NS1 and NS2, of respiratory syncytial virus (RSV) are critically required for RSV virulence. Together, they strongly suppress the type I interferon (IFN)-mediated innate immunity of the host cells by degrading or inhibiting multiple cellular factors required for either IFN induction or response pathways, including RIG-I, IRF3, IRF7, TBK1 and STAT2. Here, we provide evidence for the existence of a large and heterogeneous degradative complex assembled by the NS proteins, which we named "NS-degradasome" (NSD). The NSD is roughly ~300-750 kD in size, and its degradative activity was enhanced by the addition of purified mitochondria in vitro. Inside the cell, the majority of the NS proteins and the substrates of the NSD translocated to the mitochondria upon RSV infection. Genetic and pharmacological evidence shows that optimal suppression of innate immunity requires mitochondrial MAVS and mitochondrial motility. Together, we propose a novel paradigm in which the mitochondria, known to be important for the innate immune activation of the host, are also important for viral suppression of the innate immunity.

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“…Mitochondria, ER, and other organelles are often found in specific intracellular locations that correlate with positions of microtubules (Franke et al, 1978;Ball and Singer, 1982;Lee and Chen, 1988) or of intermediate filaments (Hirokawa, 1982;Chen, 1988). Organelles have been observed to exhibit saltatory motion characteristic of transport along cytoskeletal components (Adams, 1982;Aufderheide, 1977).…”

mentioning

confidence: 99%

Nuclear and mitochondrial inheritance in yeast depends on novel cytoplasmic structures defined by the MDM1 protein

McConnell¹

1992

Trends in Cell Biology

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Mitochondria are associated with microtubules and not with intermediate filaments in cultured fibroblasts.

Cited by 205 publications

References 45 publications

Microtubule-dependent control of cell shape and pseudopodial activity is inhibited by the antibody to kinesin motor domain.

Microtubule-dependent control of cell shape and pseudopodial activity is inhibited by the antibody to kinesin motor domain.

Viral degradasome hijacks mitochondria to suppress innate immunity

Nuclear and mitochondrial inheritance in yeast depends on novel cytoplasmic structures defined by the MDM1 protein

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