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Introduction
Emma Carpenter currently works on verifying drug targets in Plasmodium falciparum for the Pathogen Genetics Programme, Wellcome Trust Sanger Institute.
Current institution
Additional affiliations
August 2015 - December 2016
Education
October 2014 - June 2015
October 2011 - June 2014
Publications
Publications (7)
Combinations of anti-cancer drugs can overcome resistance and provide new treatments1,2. The number of possible drug combinations vastly exceeds what could be tested clinically. Efforts to systematically identify active combinations and the tissues and molecular contexts in which they are most effective could accelerate the development of combinati...
We identify the Plasmodium falciparum acetyl-coenzyme A synthetase (PfAcAS) as a druggable target, using genetic and chemical validation. In vitro evolution of resistance with two antiplasmodial drug-like compounds (MMV019721 and MMV084978) selects for mutations in PfAcAS. Metabolic profiling of compound-treated parasites reveals changes in acetyl-...
In malaria, chemical genetics is a powerful method for assigning function to uncharacterized genes. MMV085203 and GNF-Pf-3600 are two structurally related napthoquinone phenotypic screening hits that kill both blood- and sexual-stage P. falciparum parasites in the low nanomolar to low micromolar range. In order to understand their mechanism of acti...
Plasmodium parasites rely heavily on glycolysis for ATP production and for precursors for essential anabolic pathways, such as the methylerythritol phosphate (MEP) pathway. Here, we show that mutations in the Plasmodium falciparum glycolytic enzyme, phosphofructokinase ( Pf PFK9), are associated with in vitro resistance to a primary sulfonamide gly...
The search for antimalarial chemotypes with modes of action unrelated to existing drugs has intensified with the recent failure of first-line therapies across Southeast Asia. Here, we show that the trisubstituted imidazole MMV030084 potently inhibits hepatocyte invasion by Plasmodium sporozoites, merozoite egress from asexual blood stage schizonts,...
The malaria parasite Plasmodium and other apicomplexans such as Toxoplasma evolved from photosynthetic organisms and contain an essential, remnant plastid termed the apicoplast. Transcription of the apicoplast genome is polycistronic with extensive RNA processing. Yet little is known about the mechanism of apicoplast RNA processing. In plants, chlo...
The malaria parasite Plasmodium and other apicomplexans such as Toxoplasma evolved from photosynthetic organisms and contain an essential, remnant plastid termed the apicoplast. Transcription of the apicoplast genome is polycistronic with extensive RNA processing. Little is known about the mechanism of post-transcriptional processing. In plant chlo...
Questions
Question (1)
Dear all,
Having done many overnight cultures of various strains of E. coli with various vectors I was surprised to come across so much trouble in my current project.
My project uses the yeast-expression vector pPICZalpha (A,B,C) to express genes in Picha. However, the TOP10 E. coli propagating this vector (empty OR containing a gene of interest) takes 2 days (instead of 16 h) to reach a good enough concentration for mini/midi prep. Anyone else have the same issue?
I follow the protocol to the T: low salt LB, appropriate Zeocin concentration. 20 mL falcon with 5 mL of LB, shaking at 37C. On one occasion I checked the OD before miniprep, it had a good value, but the miniprep yield was poor. As far as I can tell, pPICZalpha is not a low-copy number plasmid.
My solution is simply to grow the bacteria for 2 days, so it's not a disaster, just a waste of time. If anyone had a similar problem and managed to solve it, let me know!
All the best,
Emma
