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Houra Merrikh
Assistant Professor

Website
Email: merrikh@uw.edu
Phone: (206)221-1286
Office Location: Health Sciences, J-205
Campus Box: 357735

 

 

 

 

 

 

 

 

Research:

Impediments such as breaks, DNA binding proteins, and transcription, can stall the DNA replication machinery, resulting in genomic instability, mutagenesis, and reduced fitness. The long-term goal of the Merrikh lab is to understand how these encounters influence the genomes, physiology and evolution of bacteria.

In particular, the Merrikh lab is currently interested in the consequences of the collisions between DNA replication and transcription machineries. Using a variety of approaches and cutting edge technology in the model system Bacillus subtilis (a Gram-positive bacterium), Dr. Merrikh's research group is investigating the mechanisms that are activated in response to replication-transcription conflicts and their long term evolutionary implications. The strategies used by B. subtilis are anticipated to be conserved in other Gram-positive bacteria, including the harmful pathogens Staphylococcus aureus, Clostridium difficile, Enterococcus faecalis, Listeria monocytogenes, and Streptococcus pneumonia. Furthermore, because replication conflicts occur in all life forms, the basic strategies used to deal with these problems may be conserved across species.

Dr. Merrikh received her Ph.D. from Brandeis University in 2009 and was a NIH postdoctoral fellow at the Massachusetts Institute of Technology until 2011. Dr. Merrikh is one of the recipients of the 2013 NIH Director's New Innovator Awards, which was granted in support of her ongoing work investigating the impact of replication-transcription conflicts on bacterial evolution.

Selected Publications:

Paul S, Million-Weaver S, Cattopadhyay S, Sokurenko E, and Merrikh H. Accelerated gene evolution through replication-transcription conflicts. Nature. 2013 Mar 28;495(7442):512-5.

Merrikh H, Zhang Y, Grossman AD and Wang JD. Replication-transcription conflicts in bacteria. Nature Reviews Microbiology. 2012 Jun; 10(7):449-58.

Merrikh H and Grossman AD. Control of the replication initiator DnaA by an anti-cooperativity factor. Mol Microbiol. 2011 Oct;82(2):434-46.

Lilah Rahn-Lee, Merrikh H, Grossman AD and Losick R. The Sporulation Protein SirA Inhibits the Binding of DnaA to the Origin of Replication by Contacting a Patch of Clustered Amino Acids. J Bacteriology. 2011 Mar;193(6):1302-7.

Merrikh H*, Machon C*, Grainger WH, Grossman AD and Soultanas P. Replication-transcription conflicts at rRNA genes lead to replication restart in vivo. Nature. 2011 Feb 24;470(7335):554-7. * Equal contribution.

Smits WK*, Merrikh H*, Bonilla CY and Grossman AD. Association of the helicase loader proteins DnaB and DnaD with targets of the initiator protein DnaA in Bacillus subtilis. J Bacteriology. 2011 Feb;193(3):640-8. * Equal contribution.

Merrikh H, Ferrazzoli AE, Lovett ST. Growth phase and ppGpp control of IraD, a regulator of RpoS stability, in Escherichia coli. J Bacteriology. 2009 Dec;191(24):7x436-46.

Goranov AI, Breier AM, Merrikh H, and Grossman AD. YabA of Bacillus subtilis controls DnaA-mediated replication initiation but not the transcriptional response to replication stress. Mol Microbiol. 2009 Oct;74(2):454-66.

Merrikh H, Ferrazzoli AE, Bougdour A, Olivier-Mason A, Lovett ST. A DNA damage response in Escherichia coli involving the alternative sigma factor, RpoS. Proc Natl Acad Sci USA. 2009 Jan 13;106(2):611-6

 


 

Department of Microbiology · University of Washington · Box 357735 · Seattle WA 98195-7735

phone: (206) 543-5824 · fax: (206) 543-8297 · micro@u.washington.edu