ArticleCytoskeleton (Hoboken, N.J.)2013
Dictyostelium discoideum SecG interprets cAMP-mediated chemotactic signals to influence actin organization.
Article in Cytoskeleton (Hoboken, N.J.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
2 citing papers in PubMed, 4 citations in OpenAlex.
- ATP levels influence cell movement during the mound phase in Dictyostelium discoideum as revealed by ATP visualization and simulation.FEBS open bio · 2022Article
- The C Isoform of Dictyostelium Tetraspanins Localizes to the Contractile Vacuole and Contributes to Resistance against Osmotic Stress.PloS one · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Tight control of actin cytoskeletal dynamics is essential for proper cell function and survival. Arf nucleotide binding-site opener (ARNO), a mammalian guanine nucleotide exchange factor for Arf, has been implicated in actin cytoskeletal regulation but its exact role is still unknown. To explore the role of ARNO in this regulation as well as in actin-mediated processes, the Dictyostelium discoideum homolog, SecG, was examined. SecG peaks during aggregation and mound formation. The overexpression of SecG arrests development at the mound stage. SecG overexpressing (SecG OE) cells fail to stream during aggregation. Although carA is expressed, SecG OE cells do not chemotax toward cAMP, indicating SecG is involved in the cellular response to cAMP. This chemotactic defect is specific to cAMP-directed chemotaxis, as SecG OE cells chemotax to folate without impairment and exhibit normal cell motility. The chemotactic defects of the SecG mutants may be due to an impaired cAMP response as evidenced by altered cell polarity and F-actin polymerization after cAMP stimulation. Cells overexpressing SecG have increased filopodia compared to wild type cells, implying that excess SecG causes abnormal organization of F-actin. The general function of the cytoskeleton, however, is not disrupted as the SecG OE cells exhibit proper cell-substrate adhesion. Taken together, the results suggest proper SecG levels are needed for appropriate response to cAMP signaling in order to coordinate F-actin organization during development.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.