Secrets of a successful pathogen: legionella resistance to progression along the autophagic pathway.
Secrets of a successful pathogen: legionella resistance to progression along the autophagic pathway.
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DOI：
10.3389/fmicb.2011.00138
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发表时间：
2011
影响因子：
5.2
通讯作者：
Swanson MS
中科院分区：
文献类型：
--
作者：
Joshi AD;Swanson MS
为了在吞噬细胞内增殖，嗜肺军团菌依靠IV型分泌来调节宿主细胞通路。自噬是一种进化上保守的降解途径，它捕获并转移各种微生物到溶酶体。含有嗜肺乳杆菌的液泡和自噬体的生物发生有几个共同的特征，包括内质网（ER）衍生的膜，宿主gtpase Rab1， Arf1和Sar1的贡献，以及溶酶体的最终归宿。我们讨论了形态学、分子遗传学和免疫学数据来支持这一模型，即尽管A/J小鼠巨噬细胞在自噬体膜内有效地吞噬嗜肺乳杆菌，但IV型效应蛋白DrrA/SidM、LidA和RalF延长了与内质网的关联。通过抑制立即传递到溶酶体，细菌在未成熟的自噬体液泡中持续存在一段时间，足以分化成耐酸的复制形式。随后IV型效应物LepB的分泌释放阻滞自噬体成熟，适应的后代继续在自噬溶酶体内复制。因此，嗜肺乳杆菌可以作为一种遗传学工具来分析巨噬细胞自噬途径的募集和功能。
To proliferate within phagocytes, Legionella pneumophila relies on Type IV secretion to modulate host cellular pathways. Autophagy is an evolutionarily conserved degradative pathway that captures and transfers a variety of microbes to lysosomes. Biogenesis of L. pneumophila-containing vacuoles and autophagosomes share several features, including endoplasmic reticulum (ER)-derived membranes, contributions by the host GTPases Rab1, Arf1 and Sar1, and a final destiny in lysosomes. We discuss morphological, molecular genetic, and immunological data that support the model that, although A/J mouse macrophages efficiently engulf L. pneumophila within autophagosomal membranes, the Type IV effector proteins DrrA/SidM, LidA, and RalF prolong association with the ER. By inhibiting immediately delivery to lysosomes, the bacteria persist in immature autophagosomal vacuoles for a period sufficient to differentiate into an acid-resistant, replicative form. Subsequent secretion of the Type IV effector LepB releases the block to autophagosome maturation, and the adapted progeny continue to replicate within autophagolysosomes. Accordingly, L. pneumophila can be exploited as a genetic tool to analyze the recruitment and function of the macrophage autophagy pathway.
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影响因子：
3.4
作者：
Amer, AO;Swanson, MS
通讯作者：
Swanson, MS
影响因子：
13.3
作者：
Cremer TJ;Amer A;Tridandapani S;Butchar JP
通讯作者：
Butchar JP
DOI：
10.1073/pnas.0601838103
发表时间：
2006-09-26
影响因子：
11.1
作者：
Checroun, Claire;Wehrly, Tara D.;Celli, Jean
通讯作者：
Celli, Jean
影响因子：
3.1
作者：
Derré, I;Isberg, RR
通讯作者：
Isberg, RR
影响因子：
4
作者：
Chen, Yongqiang;Klionsky, Daniel J.
通讯作者：
Klionsky, Daniel J.