Cytoplasmic streaming in characean cells: role of subcortical fibrils

1980 ◽  
Vol 58 (7) ◽  
pp. 760-765 ◽  
Author(s):  
Eiji Kamitsubo
Keyword(s):  
Electrical Stimulation ◽  
Experimental Evidence ◽  
Cytoplasmic Streaming ◽  
Motive Force ◽  
Microbeam Irradiation ◽  
Subcortical Fibrils

Three or four parallel fibrils of ca. 0.1 μm in width attached to each file of chloroplasts in intact internodal cells generate the motive force for cytoplasmic streaming. Experimental evidence for this conclusion is drawn from experiments in which fibrillar motion and streaming are interrupted by centrifugation, microbeam irradiation, and electrical stimulation. The role of Pb2+ in preventing cessation of cytoplasmic streaming after electrical stimulation is interpreted in terms of localized changes in viscosity of the cytoplasm.

scholarly journals Role of Proton Motive Force in Photoinduction of Cytoplasmic Streaming in Vallisneria Mesophyll Cells

Plants ◽  
2020 ◽  
Vol 9 (3) ◽  
pp. 376
Author(s):  
Akiko Harada ◽  
Yoshiji Okazaki ◽  
Toshinori Kinoshita ◽  
Reiko Nagai ◽  
Shingo Takagi
Keyword(s):  
Cytoplasmic Streaming ◽  
Red Light ◽  
Proton Motive Force ◽  
Motive Force ◽  
Activation Mechanism ◽  
Dependent Manner ◽  
Mesophyll Cells ◽  
P Type ◽  
Exchange Activity

In mesophyll cells of the aquatic monocot Vallisneria, red light induces rotational cytoplasmic streaming, which is regulated by the cytoplasmic concentration of Ca2+. Our previous investigations revealed that red light induces Ca2+ efflux across the plasma membrane (PM), and that both the red light-induced cytoplasmic streaming and the Ca2+ efflux are sensitive to vanadate, an inhibitor of P-type ATPases. In this study, pharmacological experiments suggested the involvement of PM H+-ATPase, one of the P-type ATPases, in the photoinduction of cytoplasmic streaming. We hypothesized that red light would activate PM H+-ATPase to generate a large H+ motive force (PMF) in a photosynthesis-dependent manner. We demonstrated that indeed, photosynthesis increased the PMF and induced phosphorylation of the penultimate residue, threonine, of PM H+-ATPase, which is a major activation mechanism of H+-ATPase. The results suggested that a large PMF generated by PM H+-ATPase energizes the Ca2+ efflux across the PM. As expected, we detected a putative Ca2+/H+ exchange activity in PM vesicles isolated from Vallisneria leaves.

TESTING GOAL-DRIVEN CAPTURE BY THREAT

2019 ◽  
Author(s):  
Chris Robert Harrison Brown
Keyword(s):  
Experimental Evidence ◽  
Attentional Capture ◽  
Critical Role ◽  
Experimental Manipulation ◽  
Contingent Capture ◽  
Top Down ◽  
Affective Stimuli ◽  
Clinical Disorders ◽  
Positive Stimuli

Attention has long been characterised within prominent models as reflecting a competition between goal-driven and stimulus-driven processes. It remains unclear, however, how involuntary attentional capture by affective stimuli, such as threat-laden content, fits into such models. While such effects were traditionally held to reflect stimulus-driven processes, recent research has increasingly implicated a critical role of goal-driven processes. Here we test an alternative goal-driven account of involuntary attentional capture by threat, using an experimental manipulation of goal-driven attention. To this end we combined the classic ‘contingent capture’ and ‘emotion-induced blink’ (EIB) paradigms in an RSVP task with both positive or threatening target search goals. Across six experiments, positive and threat distractors were presented in peripheral, parafoveal, and central locations. Across all distractor locations, we found that involuntary attentional capture by irrelevant threatening distractors could be induced via the adoption of a search goal for a threatening category; adopting a goal for a positive category conversely led to capture only by positive stimuli. Our findings provide direct experimental evidence for a causal role of voluntary goals in involuntary capture by irrelevant threat stimuli, and hence demonstrate the plausibility of a top-down account of this phenomenon. We discuss the implications of these findings in relation to current cognitive models of attention and clinical disorders.

scholarly journals Experimental evidence of pathogenic role of IgG autoantibodies in IgA nephropathy

2021 ◽  
Vol 118 ◽  
pp. 102593
Author(s):  
Zina Moldoveanu ◽  
Hitoshi Suzuki ◽  
Colin Reily ◽  
Kenji Satake ◽  
Lea Novak ◽  
...  
Keyword(s):  
Experimental Evidence ◽  
Iga Nephropathy ◽  
Pathogenic Role

scholarly journals O-GlcNAcylation protein disruption by Thiamet G promotes changes on the GBM U87-MG cells secretome molecular signature

2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Maria Cecilia Oliveira-Nunes ◽  
Glaucia Julião ◽  
Aline Menezes ◽  
Fernanda Mariath ◽  
John A. Hanover ◽  
...  
Keyword(s):  
Experimental Evidence ◽  
Critical Role ◽  
Molecular Signature ◽  
Label Free ◽  
Intercellular Signaling ◽  
Tumor Aggressiveness ◽  
Signaling Axis ◽  
Literature Evidence ◽  
Therapeutic Tools

AbstractGlioblastoma (GBM) is a grade IV glioma highly aggressive and refractory to the therapeutic approaches currently in use. O-GlcNAcylation plays a key role for tumor aggressiveness and progression in different types of cancer; however, experimental evidence of its involvement in GBM are still lacking. Here, we show that O-GlcNAcylation plays a critical role in maintaining the composition of the GBM secretome, whereas inhibition of OGA activity disrupts the intercellular signaling via microvesicles. Using a label-free quantitative proteomics methodology, we identified 51 proteins in the GBM secretome whose abundance was significantly altered by activity inhibition of O-GlcNAcase (iOGA). Among these proteins, we observed that proteins related to proteasome activity and to regulation of immune response in the tumor microenvironment were consistently downregulated in GBM cells upon iOGA. While the proteins IGFBP3, IL-6 and HSPA5 were downregulated in GBM iOGA cells, the protein SQSTM1/p62 was exclusively found in GBM cells under iOGA. These findings were in line with literature evidence on the role of p62/IL-6 signaling axis in suppressing tumor aggressiveness and our experimental evidence showing a decrease in radioresistance potential of these cells. Taken together, our findings provide evidence that OGA activity may regulate the p62 and IL-6 abundance in the GBM secretome. We propose that the assessment of tumor status from the main proteins present in its secretome may contribute to the advancement of diagnostic, prognostic and even therapeutic tools to approach this relevant malignancy.

scholarly journals Microtubule–microtubule sliding by kinesin-1 is essential for normal cytoplasmic streaming in Drosophila oocytes

2016 ◽  
Vol 113 (34) ◽  
pp. E4995-E5004 ◽  
Author(s):  
Wen Lu ◽  
Michael Winding ◽  
Margot Lakonishok ◽  
Jill Wildonger ◽  
Vladimir I. Gelfand
Keyword(s):  
Cytoplasmic Streaming ◽  
Cell Types ◽  
Nurse Cells ◽  
Wild Type ◽  
Actin Cortex ◽  
Microtubule Motor ◽  
Multiple Cell ◽  
Cytoplasmic Microtubules ◽  
Two Populations

Cytoplasmic streaming in Drosophila oocytes is a microtubule-based bulk cytoplasmic movement. Streaming efficiently circulates and localizes mRNAs and proteins deposited by the nurse cells across the oocyte. This movement is driven by kinesin-1, a major microtubule motor. Recently, we have shown that kinesin-1 heavy chain (KHC) can transport one microtubule on another microtubule, thus driving microtubule–microtubule sliding in multiple cell types. To study the role of microtubule sliding in oocyte cytoplasmic streaming, we used a Khc mutant that is deficient in microtubule sliding but able to transport a majority of cargoes. We demonstrated that streaming is reduced by genomic replacement of wild-type Khc with this sliding-deficient mutant. Streaming can be fully rescued by wild-type KHC and partially rescued by a chimeric motor that cannot move organelles but is active in microtubule sliding. Consistent with these data, we identified two populations of microtubules in fast-streaming oocytes: a network of stable microtubules anchored to the actin cortex and free cytoplasmic microtubules that moved in the ooplasm. We further demonstrated that the reduced streaming in sliding-deficient oocytes resulted in posterior determination defects. Together, we propose that kinesin-1 slides free cytoplasmic microtubules against cortically immobilized microtubules, generating forces that contribute to cytoplasmic streaming and are essential for the refinement of posterior determinants.

Sign in / Sign up

Export Citation Format

Share Document