Microbiology Scientist introduction 1: ZHAO-QING LUO
本帖最后由 细菌耐药 于 2017-2-3 01:30 编辑Our laboratory is interested in understanding the mechanisms that allow microbial pathogens to survive and multiply within the hostile host cells and how host cells respond to infection. We use Legionella pneumophila, the causative agent of Legionnaires disease as a model organism. One essential pathogenic factor of this bacterium is the Dot/Icm type IV secretion system that injects approximately 300 virulence proteins (effectors) into host cells to create a niche permissive for bacterial replication. One focus of our research is to determine the function of these proteins and their roles in bacterial infection. The second focus is to examine the mechanism of the detection and response of immune cells to intracellular pathogens, particularly the signaling pathway involved in the detection of the bacterial ribosomal protein RpsL that triggers lysosomal cell death.Finally, we are interested in study the function of Fic proteins found in diverse bacteria. The long term goal of these studies is to elucidate the signal transduction pathways important for bacterial virulence, immune detection and other events important for the establishment of successful infection, such information will be invaluable not only in combating infectious diseases but also in our understanding of cell signaling in both prokaryotic and eukaryotic cells.Education Ph.D. University of Illinois at Urbana-Champaign, 2001M.S. Beijing Agricultural University, 1994B.S., Beijing Agricultural University, 1991 Awards and Recognitions Purdue University Faculty Scholar (2012-2016)Purdue College of Science Research Award (2015)NIH-NIAID Independent Scientist Award (2011-2015) Other ActivitiesPLoS Pathogens, Associate Editor (2013-)
Selected Publications:
Qiu J, Sheedlo MJ, Yu K, Tan Y, Nakayasu ES, Das C, Liu X, Luo ZQ. 2016. Ubiquitination independent of E1 and E2 enzymes by bacterial effectors. Nature. 533:120-124. PMID: 27049943 (Highlighted and commented by Nature and Nature Review Microbiology).
Sheedlo MJ†, Qiu J†, Tan Y†, Paul LN, Luo ZQ, Das C. 2015. Structural basis of substrate recognition by a bacterial deubiquitinase important for dynamics of phagosome ubiquitination. Proc. Natl. Acad. Sci. USA. 112(49):15090-5. †, equal contribution authors. PMID: 26598703
Zhu W.†, Tao L.†, Quick M.L,. Joyce J.A., Qu J.M., Luo Z.-Q. 2015. Sensing cytosolic RpsL by macrophages induces lysosomal cell death and termination of bacterial infection. PLoS Pathogens. 11(3):e1004704. doi: 10.1371/journal.ppat.1004704. eCollection 2015 Mar. †,equal contribution authors. PMID: 25738962
Hsu F†., Luo X†., Qiu J†., Teng Y.B., Jin J., Smolka M.B., Luo Z.-Q*., Mao Y*. 2014. The Legionella effector SidC defines a unique family of ubiquitin ligases important for bacterial phagosomal remodeling. Proc. Natl. Acad. Sci. USA. 111(29):10538-43. doi: 10.1073/pnas.1402605111. Epub 2014 Jul 8. †,equal contribution authors. PMID: 25006264
Hsu F., Zhu W., Brennan L., Tao L, Luo ZQ, Mao Y. 2012. Structural basis for substrate recognition by a unique Legionella phosphoinositide phosphatase. Proc. Natl. Acad. Sci. USA.109:13567-72. PMID:23150405
Tan Y. Arnold A. J. and Luo Z.-Q. 2011. Legionella pneumophila regulates the small GTPase Rab1 activity by reversible phosphorylcholination. Proc. Natl. Acad. Sci. USA. 108:21212-7 PMID: 22158903
Tan Y. and Luo Z.-Q. 2011. Legionella pneumophila SidD is a deAMPylase that modifies Rab1. Nature. 475:506-509. PMID: 21734656.
Fontana M. F., Banga S., Barry K. C., Shen X., Tan, Y., Luo Z.-Q*. and Vance E.V*.2011. Secreted bacterial effectors that inhibit host protein synthesis are critical for induction of the innate immune response to virulent Legionella pneumophila.PLoS Pathogens. 7: e1001289. PMID: 21390206
Xu L†., Shen X†., Bryan A., Banga S., Swanson M. and Luo ZQ. 2010. Inhibition of host vacuolar H+-ATPase activity by a Legionella pneumophila effector PLoS Pathogens 19;6(3):e1000822. †, equal contribution authors, PMID: 20333253
Liu Y., Gao P. Banga S. and Luo Z.-Q.2008. An in vivo gene deletion system for determining temporal requirement of bacterial virulence factors. Proc. Natl. Acad. Sci USA. 105:9385-90. (cited by Faculty 1000). PMID: 18599442
Banga, S., Gao, P., Shen X., Fiscus V., Zong W-X., Chen L. and Luo Z.-Q. 2007. Legionellapneumophila inhibits macrophage apoptosis by targeting pro-death members of the Bcl2 protein family.Proc. Natl. Acad. Sci. USA. 104: 5121-5126. PMID: 17360363 I just interested in why can he published so many Nature, PLos pathogen, and PNAS papers? Do you want to know? I found more information about him as followed.
His laboratory is interested in understanding the cellular and molecular mechanisms that allow microbial pathogens to survive and multiply within the hostile host cells. We use Legionella pneumophila, the causative agent of Legionnaires’ disease as a model organism. This bacterium is a facultative intracellular pathogen capable of growing in a vacuole within macrophages as well as fresh water amoebae. After uptake, the Legionella-containing vacuole (LCV) in its early phase evades fusion with the lysosomal network and later is transformed into a compartment with characteristics of rough endoplasmic reticulum. Essential to the biogenesis of this replicative vacuole is the Dot/Icm Type IV protein secretion system that injects a large number of effector proteins into target host cells. These effectors modulates a variety of host cellular processes, such as remodeling of phagosomal membrane, vesicular trafficking, cell death, stress response thus allowing the establishment of the replicative compartment that supports bacterial growth. Our current focus is to analyze biochemical and cell biological activities conferred by these proteins and their roles in promoting the unique trafficking of the Legionella-containing vacuole in phagocytic cells. In particular, we are interested in identification of host proteins whose activities are modulated by substrates of the Dot/Icm system and the roles of such modulation in intracellular bacterial growth.
Caption for images found in the header: Translocation of effectors into host cell by L. pneumophila in early phase of infection . Host nucleus and bacterium were labeled in red and the effector SidC was labeled in green (Left image). Note the diffusion of SidC from the bacterial phagosome. B. Formation of a large replicative vacuole by L. pneumophila in late phase of infection (Right image). In both cases, note the perinuclear localization of the vacuole. members
By using a variety of multidisciplinary methods such as bacterial genetics, cell biology and biochemistry, our studies focus on the mechanisms of how L. pneumophila modulates two cellular processes to promote its intracellular growth. The first is the apoptotic pathways. Our study showed that the bacterium inhibits apoptosis of host cells by interacting with pro- death members of the Bcl2 protein family. The second line of research in this direction is the identification of bacterial factors responsible for the induction of host anti-apoptotic genes. On the other hand, we have identified several bacterial proteins that exert toxic effects to host cells and we are characterizing the biochemical mechanisms underlying such toxicity.
The second focus of our study is the mechanisms of the biogenesis of bacterial vacuoles, particularly those underlying the recruitment of membrane materials from the endoplasmic reticulum (ER) and the inhibition of phagosome acidification by the bacterium. Our recent progress indicated that the Dot/Icm transporter substrate SidJ is required for efficient recruitment of ER proteins to the bacterial phagosome. The current goals are the elucidation of the biochemical activity of this protein and how it coordinates with other effectors to recruit ER materials. A new strategy to disrupt the host cytoskeleton by the pathogen Legionella pneumophila
01-30-2017
Title: A new strategy to disrupt the host cytoskeleton by the pathogen Legionella pneumophila
Description of the finding: A new study published in the journal PLOS Pathogens by the Luo lab reveals that the bacterial pathogen Legionella pneumophila attacks the host cell by cleaving actin, an essential component of the cytoskeleton of eukaryotic cells important for their shape and other important cellular processes. The digestion of actin is performed by a protein called RavK, one of the many virulence factors the bacterium uses to counteract the pathogen killing strategy of the host. Cleaved actin lost the ability to form polymers, which is important for its activity. Understanding the mechanism of bacterial virulence is important for the development of novel anti-infective agents and for better appreciation of host cell biology.
Yao Liu, a graduate student in the Luo lab is the first author of the paper; former graduate students Wenhan Zhu and Yunhao Tan, Ernesto S. Nakayasu at Pacific Northwest National Laboratory, Richland, WA and Christopher J. Staiger contributed to the study.
Cleavage by RavK inhibits actin polymerization. A. Cleavage by RavK inhibited actin polymerization in actin sedimentation assay.After treatment with RavK or its mutant, actin polymerization was allowed to proceed. B. Quantification of the percentage of polymerized actin versus total actin. C. Cleavage by RavK inhibited actin polymerization in a kinetic assembly assay. D. Actin used in pyrene-labeled actin polymerization assay. Groups: i, actin treated with RavK; ii, actin treated with RavKH95A; iii, actin without treatment. Lanes: I, input; P, pellet; S, supernatant.
Link to the paper: http://journals.plos.org/plospathogens/article/authors?id=10.1371/journal.ppat.1006186
细菌耐药 老师都是英文资料啊！看不懂啊。 本帖最后由 明玥 于 2017-2-3 07:09 编辑
这篇是介绍微生物专家的对吗？考验英文水平的{:1_12:}{:1_10:}
细菌耐药老师如果把英文资料翻译过来分享给我们就好了！
可惜英文基础差，看不懂。要是有翻译就好了。谢谢 可惜英文基础差，看不懂。要是有翻译就好了。谢谢 细菌耐药老师如果把英文资料翻译过来分享给我们就更好了！ 细菌耐药 发表于 2017-2-3 02:09
A new strategy to disrupt the host cytoskeleton by the pathogen Legionella pneumophila
01-30-2017
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点赞！不愧是感控大家！佩服！ 你们好优秀呀，望文声叹。{:1_10:} it's really a good method to learn the english ,know the ademic world,thank u for ur share. 开始看到英文标题，根本没敢打开，鼓足勇气打开，还是看不懂。 荒废了很多年了。。。 本帖最后由 翔宇 于 2017-2-3 11:23 编辑
keywords:Dot/Icm system ;protein RpsL ;Fic proteins
国外拍的证件照都很有范啊！
英文标题，根本没敢打开{:1_12:} 大家不要太害怕英文，我们平常就是接触太少，缺少了学习的机会，我在实验室的电脑不能打中文，于是就直接用英文发贴了，反过来一想，这恰好也是一个学习和交流英文的方式呀。
我们SIFIC是一个学术交流、讨论与提高的平台，我想，也是要学习与交流英文的。从这个意义上来说，我们也需要一些英文的贴子。
同时，在大家回复的贴子中，我也看到了英文，很欣慰！
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