Rita Eckart

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B8 Functional analysis of Coxiella burnetii effector proteins

Principal investigator
Anja Lührmann

Mentor
Roland Lang

PhD exam: 28.03.2014

Functional analysis of Coxiella burnetii effector proteins

Coxiella burnetii is a Gram-negative, obligate intracellular pathogen that causes Q-fever, a worldwide zoonotic disease. Q-fever is a mild flu-like illness, but can be associated with chronic or even fatal outcomes. C. burnetii are typically transmitted to humans by inhalation of infectious material and infection by as few as ten bacteria can result in disease.
For intracellular pathogens such as C. burnetii, manipulation of host cell pathways is important to ensure a productive infection and may play a role in establishing chronic disease. It has recently been shown that C. burnetii employs a type IV like secretion system (T4SS) that is functionally related to the Legionella pneumophila Dot/Icm system. L. pneumophila uses this T4SS to translocate effector proteins into host cells in order to manipulate the host cell.
Our group has demonstrated that several different C. burnetii proteins with ankyrin repeat-containing domains are substrates of the T4SS. Our works indicate that the T4SS effector AnkG inhibits host cell apoptosis, probably through binding to the host cell protein p32. Two other T4SS effector proteins, AnkB and AnkF, have nuclear localization when ectopically expressed, suggesting that they may affect signal transduction pathways. This study aims to initiate the investigation on how AnkB and AnkF modulate host cell processes and to analyze the function of additional anti-apoptotic effector proteins.

 

Figure: C. burnetii employs a T4SS to translocate effector proteins into host cells in order to manipulate the host cell and to survive and multiply.

 

Publications

Klingenberg, L., Eckart, R.A., Berens, C. and Lührmann, A. (2012). The Coxiella burnetii type IV secretion system substrate CaeB inhibits intrinsic apoptosis at the mitochondrial level. Cell Microbiol 15, 675-687.

Eckart, R.A, Brantl, S. and Licht, A. (2009). Search for additional targets of the transcriptional regulator CcpN from Bacillus subtilis. FEMS Microbiol Lett 299, 223-231.

Preis, H., Eckart, R.A., Gudipati, R.K., Heidrich, N.and Brantl, S. (2009). CodY activates transcription of a small RNA in Bacillus subtilis. J Bacteriol 191, 5446-5457.

 

Presentations

July 2013 5th Annual Retreat, Erlangen School of Molecular Communication, Kloster Banz, Bad Staffelstein, Germany
Intracellular trafficking of the Coxiella burnetii effector AnkG
Talk
     
July 2012 4th Annual Retreat, Erlangen School of Molecular Communication, Kloster Banz, Bad Staffelstein, Germany
Characterizing the anti-apoptotic activity of the Coxiella burnetii effector AnkG - Interaction between AnkG and p32
Talk
     
October 2011 First International SFB 796 Conference: Mechanisms of viral host cell manipulations: from plants to humans, Bamberg, Germany
Characterizing the anti-apoptotic activity of the Coxiella burnetii effector AnkG
Poster
     
July 2011 3rd Annual Retreat, Erlangen School of Molecular Communication, Kloster Banz, Bad Staffelstein, Germany
Characterizing the anti-apoptotic activity of the Coxiella burnetii effector AnkG
Talk and Poster
     
September 2010 2nd Annual Retreat, Erlangen School of Molecular Communication, Kloster Banz, Bad Staffelstein, Germany
Inhibition of host-cell-apoptosis by the obligate intracellular pathogen Coxiella burnetii using the T4SS Effector protein AnkG
Talk
     
October 2008 7th Symposium on Mechanisms of Gene Regulation, Kassel, Germany
Transcriptional repressor CcpN from Bacillus subtilis is able to act as an activator at the thyB promoter.
Poster