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Actin‐based motility allows Listeria monocytogenes Listeria monocytogenesListeria monocytogenes to avoid autophagy in the macrophage cytosol

机译:基于肌动蛋白的运动允许 李斯特菌单核细胞增生 单核细胞增生 Histeria单核细胞增生,以避免巨噬细胞胞浆中的自噬

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Abstract > <fc> <fi>Listeria monocytogenes</fi> </fc> grows in the host cytosol and uses the surface protein ActA to promote actin polymerisation and mediate actin‐based motility. ActA, along with two secreted bacterial phospholipases C, also mediates avoidance from autophagy, a degradative process that targets intracellular microbes. Although it is known that ActA prevents autophagic recognition of <fc> <fi>L.?monocytogenes</fi> </fc> in epithelial cells by masking the bacterial surface with host factors, the relative roles of actin polymerisation and actin‐based motility in autophagy avoidance are unclear in macrophages. Using pharmacological inhibition of actin polymerisation and a collection of actA mutants, we found that actin polymerisation prevented the colocalisation of <fc> <fi>L.?monocytogenes</fi> </fc> with polyubiquitin, the autophagy receptor p62, and the autophagy protein LC3 during macrophage infection. In addition, the ability of <fc> <fi>L.?monocytogenes</fi> </fc> to stimulate actin polymerisation promoted autophagy avoidance and growth in macrophages in the absence of phospholipases C. Time‐lapse microscopy using green fluorescent protein‐LC3 macrophages and a probe for filamentous actin showed that bacteria undergoing actin‐based motility moved away from LC3‐positive membranes. Collectively, these results suggested that although actin polymerisation protects the bacterial surface from autophagic recognition, actin‐based motility allows escape of <fc> <fi>L.?monocytogenes</fi> </fc> from autophagic membranes in the macrophage cytosol. </abstract> </span> <span class="z_kbtn z_kbtnclass hoverxs" style="display: none;">展开▼</span> </div> <div class="translation abstracttxt"> <span class="zhankaihshouqi fivelineshidden" id="abstract"> <span>机译:</span><abstract type =“main”xml:lang =“en”> <title type =“main”>抽象</ title> > <fc> <fi> histeria单核细胞元</ fi> </ fc>生长宿主细胞溶胶并使用表面蛋白抗肌肌,以促进肌动蛋白聚合和介导的基于肌动蛋白的运动性。 Acta以及两个分泌的细菌磷脂仿酶C,也介导避免自噬,靶向细胞内微生物的降解过程。虽然已知acta通过用宿主因子掩蔽细菌表面,肌动蛋白聚合和基于肌动蛋白的相对作用,acta防止上皮细胞中<fc> <fi>l.βmonocytogens的自噬识别<fc> <fi> l.? mnocytogenes </ fi> <omonocogens的自噬识别。巨噬细胞避免的动力在巨噬细胞中不清楚。使用肌动蛋白聚合的药理抑制和抗肌动酶突变体的收集,我们发现肌动蛋白聚合方法阻止了用络合剂的<Fc> <Fi>L.β/ Fi> </ Fi> </ Fi> </ Fi>的离子化。巨噬细胞感染过程中自噬受体p62和自噬蛋白Lc3。此外,<FC> <FI>L.β/ FI> </ FC>刺激肌动蛋白聚合的能力促进了在没有磷脂酶C的情况下促进巨噬细胞的自噬避免和生长。使用绿色荧光蛋白的延时显微镜-LC3巨噬细胞和丝状肌动蛋白的探针表明,经历基于肌动蛋白的运动的细菌远离LC3阳性膜。总的来说,这些结果表明,虽然肌动蛋白聚合保护免受自噬识别的自噬型识别细菌表面,但肌动蛋白的运动允许从巨噬细胞胞质溶胶中的自噬膜中逸出<fc> <fi> l.? monocytogens-/ fi> </ fc>。 </ p> </ abstract> </span> <span class="z_kbtn z_kbtnclass hoverxs" style="display: none;">展开▼</span> </div> </div> <div class="record"> <h2 class="all_title" id="enpatent33" >著录项</h2> <ul> <li> <span class="lefttit">来源</span> <div style="width: 86%;vertical-align: text-top;display: inline-block;"> <a href='/journal-foreign-15891/'>《Cellular microbiology》</a> <b style="margin: 0 2px;">|</b><span>2018年第9期</span><b style="margin: 0 2px;">|</b><span>共13页</span> </div> </li> <li> <div class="author"> <span class="lefttit">作者</span> <p id="fAuthorthree" class="threelineshidden zhankaihshouqi"> <a href="/search.html?doctypes=4_5_6_1-0_4-0_1_2_3_7_9&sertext=Cheng Mandy I.&option=202" target="_blank" rel="nofollow">Cheng Mandy I.;</a> <a href="/search.html?doctypes=4_5_6_1-0_4-0_1_2_3_7_9&sertext=Chen Chen&option=202" target="_blank" rel="nofollow">Chen Chen;</a> <a href="/search.html?doctypes=4_5_6_1-0_4-0_1_2_3_7_9&sertext=Engstr?m Patrik&option=202" target="_blank" rel="nofollow">Engstr?m Patrik;</a> <a href="/search.html?doctypes=4_5_6_1-0_4-0_1_2_3_7_9&sertext=Portnoy Daniel A.&option=202" target="_blank" rel="nofollow">Portnoy Daniel A.;</a> <a href="/search.html?doctypes=4_5_6_1-0_4-0_1_2_3_7_9&sertext=Mitchell Gabriel&option=202" target="_blank" rel="nofollow">Mitchell Gabriel;</a> </p> <span class="z_kbtnclass z_kbtnclassall hoverxs" id="zkzz" style="display: none;">展开▼</span> </div> </li> <li> <div style="display: flex;"> <span class="lefttit">作者单位</span> <div style="position: relative;margin-left: 3px;max-width: 639px;"> <div class="threelineshidden zhankaihshouqi" id="fOrgthree"> <p>Department of Molecular and Cell BiologyUniversity of CaliforniaBerkeley CA USA;</p> <p>Department of Molecular and Cell BiologyUniversity of CaliforniaBerkeley CA USA;</p> <p>Department of Molecular and Cell BiologyUniversity of CaliforniaBerkeley CA USA;</p> <p>Department of Molecular and Cell BiologyUniversity of CaliforniaBerkeley CA USA;</p> <p>Department of Molecular and Cell BiologyUniversity of CaliforniaBerkeley CA USA;</p> </div> <span class="z_kbtnclass z_kbtnclassall hoverxs" id="zhdw" style="display: none;">展开▼</span> </div> </div> </li> <li > <span class="lefttit">收录信息</span> <span style="width: 86%;vertical-align: text-top;display: inline-block;"></span> </li> <li> <span class="lefttit">原文格式</span> <span>PDF</span> </li> <li> <span class="lefttit">正文语种</span> <span>eng</span> </li> <li> <span class="lefttit">中图分类</span> <span><a href="https://www.zhangqiaokeyan.com/clc/173.html" title="普通生物学">普通生物学;</a></span> </li> <li class="antistop"> <span class="lefttit">关键词</span> <p style="width: 86%;vertical-align: text-top;"> <a style="color: #3E7FEB;" href="/search.html?doctypes=4_5_6_1-0_4-0_1_2_3_7_9&sertext=ActA&option=203" rel="nofollow">ActA;</a> <a style="color: #3E7FEB;" href="/search.html?doctypes=4_5_6_1-0_4-0_1_2_3_7_9&sertext=bacteria&option=203" rel="nofollow">bacteria;</a> <a style="color: #3E7FEB;" href="/search.html?doctypes=4_5_6_1-0_4-0_1_2_3_7_9&sertext=PLCs&option=203" rel="nofollow">PLCs;</a> <a style="color: #3E7FEB;" href="/search.html?doctypes=4_5_6_1-0_4-0_1_2_3_7_9&sertext=ubiquitin&option=203" rel="nofollow">ubiquitin;</a> <a style="color: #3E7FEB;" href="/search.html?doctypes=4_5_6_1-0_4-0_1_2_3_7_9&sertext=xenophagy&option=203" rel="nofollow">xenophagy;</a> </p> <div class="translation"> 机译:acta;细菌;plcs;泛素;xeoophagy; 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