Control of plasma membrane-associated actin polymerization specifies the pattern of the cell wall in xylem vessels.
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ABSTRACT:
PROVIDER: PRJNA1207997 | ENA |
REPOSITORIES: ENA
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Project description:Cell wall patterning is central to determining the shape and function of plant cells. Protoxylem and metaxylem vessel cells deposit banded and pitted cell walls, respectively, which enable their distinctive water transport capabilities, but the mechanisms that specify which cell wall pattern is laid down remain unknown. Here, we show that the pitted cell wall pattern in metaxylem vessels is specified by transcriptional control of actin polymerization. A newly isolated allele of KNOTTED-like homeobox transcription factor 7 (KNAT7) was associated with the formation of banded cell walls in metaxylem vessels. To identify the genes responsible for altering the cell wall pattern in knat7 xylem vessels, we performed an RNA-seq analysis of knat7. We used in vitro cultures of hypocotyls and cotyledons because the population of differentiating xylem cells in intact roots is tiny and these methods efficiently induce ectopic differentiation of xylem vessel elements. Formin Homology Domain-Containing Protein 11 (FH11) was upregulated in knat7 metaxylem, but expressed only in protoxylem vessels in wild-type plants. Loss of FH11 suppressed the knat7 phenotype. Conversely, ectopic overexpression of FH11 in metaxylems mimicked the knat7 phenotype. FH11 function required its plasma membrane anchoring and the actin polymerization activity. Actin polymerization by FH11 at the plasma membrane caused the dispersion of activated ROP GTPases, the determinant of pit formation. These results suggest that decontrol of actin polymerization at the plasma membrane abolishes the pitted cell wall formation and promotes the formation of banded cell walls in metaxylem vessels. This study unveils the importance of the proper control of actin polymerization on cell wall pattern specification.
2025-01-15 | GSE286145 | GEO
Project description:Patterned cell wall deposition is crucial for cell shapes and functions. In Arabidopsis xylem vessels, ROP11 GTPase locally inhibits cell wall deposition through microtubule disassembly, inducing pits in cell walls. Here, we show that an additional ROP signaling pathway promotes cell wall growth at pit boundaries. Two proteins, Boundary of ROP domain1 (BDR1) and Wallin (WAL), localize to pit boundaries and regulate cell wall growth. WAL interacts with F-actin and promotes actin assembly at pit boundaries while BDR1 is a ROP effector. BDR1 interacts with WAL, suggesting that WAL could be recruited to the plasma membrane by a ROP-dependent mechanism. These results demonstrate that BDR1 and WAL mediate a ROP-actin pathway that shapes pit boundaries. The study reveals a distinct machinery in which two closely associated ROP pathways oppositely regulate cell wall deposition patterns for the establishment of tiny but highly specialized cell wall domains.
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Project description:Megakaryoblastic leukemia 1 (MKL1) promotes the regulation of essential cell processes, including actin cytoskeletal dynamics by co-activating serum response factor. Recently, the first human case with MKL1 deficiency, leading to a novel primary immunodeficiency, was identified. We report a second family with two siblings with a homozygous frameshift mutation in MKL1. The index case deceased as an infant from progressive and severe pneumonia by Pseudomonas aeruginosa and poor wound healing. The younger sib was preemptively transplanted shortly after birth. The immunodeficiency was marked by a pronounced actin polymerization defect and a strongly reduced motility and chemotactic response by MKL1-deficient neutrophils. Apart from the lack of MKL1, subsequent proteomic and transcriptomic analyses of patient neutrophils revealed actin and several actin-related proteins to be downregulated, confirming a role for MKL1 as transcriptional co-regulator. Degranulation was enhanced upon suboptimal neutrophil activation, while production of reactive oxygen species was normal. Neutrophil adhesion was intact but without proper spreading. The latter could explain the observed failure in firm adherence and transendothelial migration under flow conditions. No apparent defect in phagocytosis and bacterial killing was found. Also monocyte-derived macrophages showed intact phagocytosis; lymphocyte counts and proliferative capacity were normal. Non-hematopoietic primary patient fibroblasts demonstrated defective differentiation into myofibroblasts but normal migration and filamentous actin (F-actin) content, most probably due to compensatory mechanisms of MKL2, which is not expressed in neutrophils. Our findings extend current insight into the severe immune dysfunction in MKL1 deficiency, with cytoskeletal dysfunction and defective extravasation of neutrophils as most prominent features.
2020-03-16 | GSE134644 | GEO
Project description:Actin polymerization by WASp limits nuclear envelope rupture and inflammation in macrophages I
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Project description:Characterization of open chromatin sensitive to actin polymerization using DSP-MNase-DNA-seq
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Project description:The mechanisms underlying cancer metastasis remain poorly understood. Here, we report that TFAM deficiency rapidly and stably induced spontaneous lung metastasis in mice with liver cancer. Interestingly, unexpected polymerization of nuclear actin was observed in TFAM-knockdown HCC cells when cytoskeleton was examined. Polymerization of nuclear actin is causally linked to the high-metastatic ability of HCC cells by modulating chromatin accessibility and coordinating the expression of genes associated with extracellular matrix remodeling, angiogenesis, and cell migration. Mechanistically, TFAM deficiency blocked the TCA cycle and increased the intracellular malonyl-CoA levels. Malonylation of mDia2, which drives actin assembly, promotes its nuclear translocation. Importantly, inhibition of malonyl-CoA production or nuclear actin polymerization significantly impeded the spread of HCC cells in mice. Moreover, TFAM was significantly downregulated in metastatic HCC tissues and was associated with overall survival and time to tumor recurrence of HCC patients. Taken together, our study connects mitochondria to the metastasis of human cancer via uncovered mitochondria-to-nucleus retrograde signaling, indicating that TFAM may serve as an effective target to block HCC metastasis.
2022-06-23 | MTBLS4307 | MetaboLights
Project description:CD4 T helper cells can differentiate to several types of cells like Th1, Th2, Th17 and Treg. This process is directed by cytokines and activation of T cells by specific antigens. This process has its own plasticity and it is directed by epigenetic changes allowing cells to develop and differentiate. In this experiment, we wanted to explore the binding pattern of EZH2 in the first 24 hours of Th cells activation and differentiation side by side with VAV1 binding pattern to understand the importance of actin polymerization factors in this process.
2021-08-28 | E-MTAB-9524 | biostudies-arrayexpress
Project description:Trichloroethylene (TCE) is primarily used as an industrial degreasing agent and has been in use since the 1940s. TCE is released into the soil, surface, and groundwater. From an environmental and regulatory standpoint more than half of Superfund hazardous waste sites on the National Priority List are contaminated with TCE. Occupational exposure to TCE occurs primarily via inhalation, while environmental TCE exposure also occurs through ingestion of contaminated drinking water. Current literature links TCE exposure to various adverse health effects including cardiovascular toxicity. Current studies aiming to address developmental cardiovascular toxicity utilized rodent and avian models with the majority of studies using relatively higher parts per million (ppm; mg/L) doses. In this study to further investigate developmental cardiotoxicity of TCE, zebrafish embryos were treated with 0, 10, 100, or 500 parts per billion (ppb; μg/L) TCE during embryogenesis and/or through early larval stages. After the appropriate exposure period, angiogenesis, F-actin polymerization, and mitochondrial function were assessed. A significant dose response decrease in angiogenesis, F-actin polymerization, and mitochondrial function was observed. To further complement this data, a transcriptomic profile of zebrafish larvae was completed to identify gene alterations associated with the 10 ppb TCE exposure. Results from the transcriptomic data revealed that an embryonic TCE exposure caused significant changes in genes associated with cardiovascular disease, cancer, and organismal injury and abnormalities with a number of targets in the FAK signaling pathway. Overall, results from our study further support TCE as a developmental cardiovascular toxicant and continued priority for environmental regulation.
2016-02-01 | GSE72918 | GEO
Project description:MKL1 deficiency results in a severe neutrophil motility defect due to impaired actin polymerization
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Project description:Mitochondrial damage (MtD) represents a dramatic change in cellular homeostasis, necessitating metabolic changes and stimulating mitophagy. One rapid response to MtD is rapid peri-mitochondrial actin polymerization, termed ADA (acute damage-induced actin). The activation mechanism for ADA is unknown. Here, we use mitochondrial depolarization or the complex I inhibitor metformin to induce ADA. We show that two parallel signaling pathways are required for ADA. In one pathway, increased cytosolic calcium activates in turn PKC-β, Rac, WAVE regulatory complex, and Arp2/3 complex. In the other pathway, a drop in cellular ATP activates in turn AMPK (through LKB1), Cdc42, and FMNL formins. We also identify putative guanine nucleotide exchange factors for Rac and Cdc42, Trio and Fgd1 respectively, whose phosphorylation states increase upon mitochondrial depolarization and whose suppression inhibits ADA. The depolarization-induced calcium increase is dependent on the mitochondrial sodium-calcium exchanger NCLX, suggesting initial mitochondrial calcium efflux. We also show that ADA inhibition results in enhanced mitochondrial shape changes upon mitochondrial depolarization, suggesting that ADA inhibits these shape changes. These depolarization-induced shape changes are not fragmentation but a circularization of the inner mitochondrial membrane, dependent on the inner mitochondrial membrane protease Oma1. ADA inhibition increases proteolytic processing of an Oma1 substrate, the dynamin GTPase Opa1. These results show that ADA requires the combined action of Arp2/3 complex and formin proteins to polymerize a network of actin filaments around mitochondria, and that the ADA network inhibits the rapid mitochondrial shape changes that occur upon mitochondrial depolarization.
2022-03-15 | PXD031699 | Pride