Fixation‐induced cell blebbing on spread cells inversely correlates with phosphatidylinositol 4,5‐bisphosphate level in the plasma membrane

Zhao, Siyuan; Liao, Huanhuan; Ao, Meiying; Wu, Li; Zhang, Xiaojun; Chen, Yong

doi:10.1016/j.fob.2014.02.003

Cited by 24 publications

(22 citation statements)

References 35 publications

(40 reference statements)

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“…It has been suggested that many cytoskeleton‐interacting proteins reversibly bind PIP2 at the plasma membrane. Therefore, decreasing PIP2 level or local delocalisation could lead to destabilisation of membrane–cytoskeleton adhesions resulting in bleb formation (Zhao et al, ). The results shown here suggest that EhRho1 modulates PI3 kinase activity in E. histolytica cells.…”

Section: Resultsmentioning

confidence: 99%

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EhRho1 regulates plasma membrane blebbing through PI3 kinase inEntamoeba histolytica

Bharadwaj

Arya

Mansuri

et al. 2017

Cellular Microbiology

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The protozoan parasite Entamoeba histolytica causes amoebiasis, a major public health problem in developing countries. Motility of E. histolytica is important for its pathogenesis. Blebbing is an essential process contributing to cellular motility in many systems. In mammalian cells, formation of plasma membrane blebs is regulated by Rho-GTPases through its effectors, such as Rho kinase, mDia1, and acto-myosin proteins. In this study, we have illuminated the role of EhRho1 in bleb formation and motility of E. histolytica. EhRho1 was found at the site of bleb formation in plasma membrane of trophozoites. Overexpression of mutant EhRho1 defective for Guanosine triphosphate (GTP)-binding or down-regulating EhRho1 by antisense RNA resulted in reduced blebbing and motility. Moreover, serum-starvation reduced blebbing that was restored on serum-replenishment. Lysophosphatidic acid treatment induced bleb formation, whereas wortmannin inhibited the process. In all these cases, concentration of GTP-EhRho1 (active) and Phosphatidylinositol 4,5-bisphosphate (PIP2) inversely correlated with the level of plasma membrane blebbing. Our study suggests the role of EhRho1 in blebbing and bleb-based motility through PI3 kinase pathway in E. histolytica.

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Section: Resultsmentioning

confidence: 99%

“…It has been shown that plasma membrane PIP2 affects actin cytoskeleton as well as blebbing in Dictyostelium discoideum and human umbilical vein endothelial cells. Depletion of PIP2 from plasma membrane enhanced bleb formation, whereas sequestering of PIP2 resulted in reduced bleb formation (Zatulovskiy & Kay, ; Zhao et al, ).…”

Section: Discussionmentioning

confidence: 99%

EhRho1 regulates plasma membrane blebbing through PI3 kinase inEntamoeba histolytica

Bharadwaj

Arya

Mansuri

et al. 2017

Cellular Microbiology

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“…Human THP-1 monocytic leukemia cells, purchased from the Cell Bank of the Chinese Academy of Sciences (Shanghai, China), were differentiated to macrophages by a phorbol ester (phorbo-12-myristate-13-acetate, PMA) as previously reported (Zhao et al 2014). THP-1 cells were routinely cultured in DMEM media supplemented with 10% FBS, 100 U/ml penicillin, 100 lg/ml streptomycin, and 2 mM L-glutamine.…”

Section: Monocytes/macrophages and Cell Culturesmentioning

confidence: 99%

Phosphatidylethanolamine Deficiency ImpairsEscherichia coliAdhesion by Downregulating Lipopolysaccharide Synthesis, Which is Reversible by High Galactose/Lactose Cultivation

Chen

Sun

et al. 2017

Cell Communication & Adhesion

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As the initiation step of bacterial infection or biofouling, bacterial adhesion on cells or substrates is generally an optimal target for antibacterial design. Phosphatidylethanolamine (PE) is the principal phospholipid in bacteria, and its function in bacterial adhesion remains unclear. In this study, four E. coli strains including two PE-deficient mutants (PEPC and PEPCstrains) and two PE-containing wild-type controls (PE PC strains) were recruited to investigate the influence of PE deficiency on bacterial adhesion. We found that PE deficiency could impair E. coli adhesion on macrophages (human THP-1-derived and mouse RAW264.7 macrophages) or glass coverslips by downregulating lipopolysaccharide (LPS) biosynthesis, which could be reversible by high galactose/lactose but not glucose cultivation. The data imply that PE play important role in bacterial adhesion probably via affecting LPS biosynthesis and suggest that targeting PE biosynthesis is also a potential antibacterial strategy.

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“…The observation that blebs extend at cortical regions that possess less PIP2 is consistent with the results of the membrane tethering experiments, which indicated that PIP2 increases the strength of adhesion between the actin cortex and cell membrane [ 38 ]. Recent observations of blebs in Xenopus primordial germ cells and of fixation-induced blebs in human leukemia cells also indicate the important role of PIP2 in bleb formation [ 41 , 42 ].…”

Section: Discussionmentioning

confidence: 99%

Microtubule-Mediated Inositol Lipid Signaling Plays Critical Roles in Regulation of Blebbing

2015

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Cells migrate by extending pseudopods such as lamellipodia and blebs. Although the signals leading to lamellipodia extension have been extensively investigated, those for bleb extension remain unclear. Here, we investigated signals for blebbing in Dictyostelium cells using a newly developed assay to induce blebbing. When cells were cut into two pieces with a microneedle, the anucleate fragments vigorously extended blebs. This assay enabled us to induce blebbing reproducibly, and analyses of knockout mutants and specific inhibitors identified candidate molecules that regulate blebbing. Blebs were also induced in anucleate fragments of leukocytes, indicating that this assay is generally applicable to animal cells. After cutting, microtubules in the anucleate fragments promptly depolymerized, followed by the extension of blebs. Furthermore, when intact cells were treated with a microtubule inhibitor, they frequently extended blebs. The depolymerization of microtubules induced the delocalization of inositol lipid phosphatidylinositol 3,4,5-trisphosphate from the cell membrane. PI3 kinase-null cells frequently extended blebs, whereas PTEN-null cells extended fewer blebs. From these observations, we propose a model in which microtubules play a critical role in bleb regulation via inositol lipid metabolism.

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Fixation‐induced cell blebbing on spread cells inversely correlates with phosphatidylinositol 4,5‐bisphosphate level in the plasma membrane

Cited by 24 publications

References 35 publications

EhRho1 regulates plasma membrane blebbing through PI3 kinase inEntamoeba histolytica

EhRho1 regulates plasma membrane blebbing through PI3 kinase inEntamoeba histolytica

Phosphatidylethanolamine Deficiency ImpairsEscherichia coliAdhesion by Downregulating Lipopolysaccharide Synthesis, Which is Reversible by High Galactose/Lactose Cultivation

Microtubule-Mediated Inositol Lipid Signaling Plays Critical Roles in Regulation of Blebbing

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