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11 results for “Formin”
Distinct roles of the Chlamydia trachomatis effectors TarP and TmeA in the regulation of formin and Arp2/3 during entry
<p>The obligate intracellular pathogen Chlamydia trachomatis manipulates the host actin cytoskeleton to assemble actin-rich structures that drive pathogen entry. The recent discovery of TmeA, which, like TarP, is an invasion-associated type III effector implicated in actin remodeling, raised questions regarding the nature of their functional interaction. Quantitative live-cell imaging of actin remodeling at invasion sites revealed differences in recruitment and turnover kinetics associated with the TarP and TmeA pathways, with the former accounting for most of the robust actin dynamics at invasion sites. TarP-mediated recruitment of actin nucleators, i.e. formins and the Arp2/3 complex, was crucial for rapid actin kinetics, generating a collaborative positive feedback loop that enhanced their respective actin-nucleating activities within invasion sites. In contrast, the formin Fmn1 was not recruited to invasion sites and did not collaborate with Arp2/3 within the context of Tme-aassociated actin recruitment. Although the TarP-Fmn1-Arp2/3 signaling axis is responsible for the majority of actin dynamics, its inhibition had similar effects as the deletion of TmeA on invasion efficiency, consistent with the proposed model that TarP and TmeA act on different stages of the same invasion pathway.</p>
Distinct roles of the Chlamydia trachomatis effectors TarP and TmeA in the regulation of formin and Arp2/3 during entry
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Data from: Regulation of the formin INF2 by actin monomers and calcium-calmodulin
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Data from: Formin is associated with left-right asymmetry in the pond snail and the frog
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FHOD formin and SRF promote striated muscle development through separate pathways in C. elegans
GEO Series GSE158232. Caenorhabditis elegans. 12 samples. Type: Expression profiling by high throughput sequencing.
CDK1-formin signal confers microvillar effacement by an attaching and effacing (A/E) pathogen
GEO Series GSE142507. Caenorhabditis elegans. 2 samples. Type: Expression profiling by high throughput sequencing.
Formin 2 Links Neuropsychiatric Phenotypes At Young Age To An Increased Risk For Dementia
GEO Series GSE100070. Mus musculus. 48 samples. Type: Expression profiling by high throughput sequencing.
Evaluation of Formin Gene Status and Expression in Myeloproliferative and Myelodysplastic Disorders
ClinicalTrials.gov study NCT00687414. IPD Sharing: Not stated. Countries: 1. Publications: 0.
Effects of formin impairment on gene expression in Arabidopsis seedlings
GEO Series GSE89466. Arabidopsis thaliana. 8 samples. Type: Expression profiling by array.
Dataset raw data related to article "In-depth genetic and molecular characterization of Diaphanous Related Formin 2 (DIAPH2) and its role in the inner ear"
<p>This record contains the raw data (Exome sequencing) related to article "In-depth genetic and molecular characterization of DIAPH2 as a novel candidate gene for hearing loss"</p> <p><strong>ABSTRACT </strong></p> <p>Hereditary hearing loss is characterized by an extreme genetic heterogeneity. Nowadays, whole-exome sequencing represents a reasonably cost-effective approach for both mutational screening of known deafness genes and novel disease-gene identification. Here, we investigate the role of Diaphanous-related formin 2 (DIAPH2), coding for a protein involved in actin filament elongation, in nonsyndromic hearing loss. Using whole-exome sequencing, we found a predicted pathogenic missense variant at a conserved site in <em>DIAPH2</em>, which segregated with nonsyndromic X-linked hearing loss in an Italian family. Our immunohistochemical studies indicated that the mouse ortholog protein Diaph2 is expressed during development in the cochlea, specifically in the actin-rich stereocilia of the sensory outer hair cells. <em>In-vitro</em> studies showed a possible functional impairment of the mutant DIAPH2 protein upon RhoA-dependent activation. Finally, <em>Diaph2</em> knock-out and knock-in mice were generated by CRISPR/Cas9 technology and auditory brainstem response measurements performed at 4, 8 and 14 weeks. However, no hearing impairment was detected, possibly due to functional redundancy/compensation by other diaphanous proteins. Our findings indicate that <em>DIAPH2</em> may play a role in the inner ear; further studies are however needed to clarify the contribution of <em>DIAPH2</em> to deafness.</p> <p> </p>
Dataset related to article "In-depth genetic and molecular characterization of Diaphanous Related Formin 2 (DIAPH2) and its role in the inner ear"
<p>This record contains data (Table S1 to S4, Figure S1 to S12, File S1) related to article “In-depth genetic and molecular characterization of Diaphanous Related Formin 2 (<em>DIAPH2</em>) and its role in the inner ear” . </p> <p>Specifically, the record contains the following supplementary information to the article:</p> <p>Table S1. Coding sequence coverage of known autosomal recessive and X-linked NSHL-causing genes in exome data.</p> <p>Table S2. Prioritized variants shared between affected siblings III1 and III3.</p> <p>Table S3. CNVs shared between affected siblings III1 and III3.</p> <p>Table S4. Primers used for genetic screening of candidate genes/variants.</p> <p>Figure S1. Analysis of auditory brainstem evoked potentials in proband III3.</p> <p>Figure S2. Expression of mouse <em>Diaph2 </em>mRNA in P4 organ of Corti by RT-PCR. </p> <p>Figure S3. Diaph2 expression in E14.5 and E16.5 wild-type mouse cochlea.</p> <p>Figure S4. Evaluation of Diaph2 expression in whole-mount mouse cochleas.</p> <p>Figure S5. Diaph2 expression in P7 and P14 wild-type mouse cochlea.</p> <p>Figure S6. <em>In-silico</em> analysis of the impact of c.868A>G variant on <em>DIAPH2</em> pre-mRNA splicing.</p> <p>Figure S7. <em>In-vitro</em> analysis of the impact of c.868A>G variant on <em>DIAPH2</em> pre-mRNA splicing.</p> <p>Figure S8. <em>In-vitro</em> characterization of the effect of the c.868A>G variation on splicing using a <em>DIAPH2</em>minigene spanning exons 6 to 9.</p> <p>Figure S9. Analysis of <em>DIAPH2</em> exon 8 splicing in blood from NSHL3 family subjects.</p> <p>Figure S10. <em>In-vivo</em> analysis of <em>Diaph2</em> exon 8 splicing in the mouse cochlea.</p> <p>Figure S11. Pathogenicity prediction of the p.I290V missense variant with 8 commonly used software.</p> <p>Figure S12. DIAPH2 immunolocalization studies in basal conditions.</p> <p>File S1. Supplementary Methods</p>
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