I completed my PhD in December 2012, working alongside researchers at Rothamsted Research, focussing on the molecular mechanisms of pyrethroid and DDT insecticide resistance at the insect Voltage Gated Sodium Channel (VGSC).
In February 2013 I started a 3 year post-doctoral position in the department of Cell Physiology & Pharmacology a the University of Leicester where my research is focussed on the interaction of haem, in its ligand form, at the calcium sensitive BK channel (slo1 K+) and the ATP sensitive potassium channel (KATP).
Here is some posts of my research past and present.
Only just started at the University of Leicester, but some initial work looks at examining haem modulation of the KATP channel and explore its role in physiological conditioning of the myocardium following metabolic inhibition.
More to follow in time.
In 2009/2010, Dr Joanna Amey cloned and sequenced the sodium channel from Myzus persicae (peach potato aphid) which showed some interesting features. It was my job to try and get the protein functionally expressed to identify it as the Myzus VGSC.
Unfortunately, there have been several false starts in trying to get this thing expressed. However, the team is not short of ideas and we are trying all sorts of novel ideas to get more of an insight into this ion channel protein. More to follow on with this project.
My first topic of study has been investigating the biochemistry of pyrethroid insecticides at the voltage gated sodium channel (VGSC) and associated resistance.
To break this down further, pyrethroid insecticides make up around 20% of the world's insecticide market and remain the only safe treatment of mosquito bednets. Unfortunately, these compounds are becoming less effective due to the establishment of resistance in pest insect species. This resistance can be due to 'target site' modification i.e. the site at which pyrethroids act upon is mutated to reduce efficacy or 'increased detoxification' i.e. the pyrethroid compounds are being broken down/metabolised due to upregulation of specific genes responsible for this process.
My specific interest has been trying to see how mutations within the VGSC (target site) alter the functionality of the VGSC and in turn its effects upon the nervous system. We have studied 5 mutations at a specific site within the VGSC gene; this site is known as the classic knockdown resistance (kdr) site. 3 of these mutations have been found in established, resistant insect populations: a leucine to phenylalanine/serine/histidine at position 1014 in the gene.
Our research paper compares channel physiology between mutations and levels of resistance to two key pyrethroid compounds (permethrin and deltamethrin)