Molecular identification of tsetse fly (Diptera: Glossinidae) species based on mitochondrial DNA (COII and CytB) sequences

Tsetse fly (Diptera: Glossinidae) anti-vector measures are reliant upon accurate identification of species and their subpopulations. Two species were studied, Glossina palpalis palpalis and Glossina morsitans submorsitans using two mitochondrial DNA: cytochrome oxidase subunit II (COII) and cytochrome b (CytB). Sequencing data were used to perform phylogenetic analysis of the two reared species together with other Glossina species’ sequences from the DNA data base. For each gene, members of the same species group, palpalis or morsitans demonstrated a common ancestry and closer relatedness by belonging to one cluster. Within each species group members of the same species clustered together, an indication of common ancestry and relatedness too. Inspite of the few mixed clusters, the pattern produced in the phylogenetic trees can provide a good guide to support any other method of Glossina identification. It was recommended that evaluations be made to validate other genetic markers that can produce better resolutions to identify tsetse fly species using phylogenetic tree.Key words: Trypanosomiasis, Glossina palpalis palpalis, Glossina morsitans submorsitans, cytochrome oxidase II, cytochrome b, neighbour joining tree

Reduced Mature MicroRNA Levels in Association with Dicer Loss in Human Temporal Lobe Epilepsy with Hippocampal Sclerosis

Hippocampal sclerosis (HS) is a common pathological finding in patients with temporal lobe epilepsy (TLE) and is associated with altered expression of genes controlling neuronal excitability, glial function, neuroinflammation and cell death. MicroRNAs (miRNAs), a class of small non-coding RNAs, function as post-transcriptional regulators of gene expression and are critical for normal brain development and function. Production of mature miRNAs requires Dicer, an RNAase III, loss of which has been shown to cause neuronal and glial dysfunction, seizures, and neurodegeneration. Here we investigated miRNA biogenesis in hippocampal and neocortical resection specimens from pharmacoresistant TLE patients and autopsy controls. Western blot analysis revealed protein levels of Dicer were significantly lower in certain TLE patients with HS. Dicer levels were also reduced in the hippocampus of mice subject to experimentally-induced epilepsy. To determine if Dicer loss was associated with altered miRNA processing, we profiled levels of 380 mature miRNAs in control and TLE-HS samples. Expression of nearly 200 miRNAs was detected in control human hippocampus. In TLE-HS samples there was a large-scale reduction of miRNA expression, with 51% expressed at lower levels and a further 24% not detectable. Primary transcript (pri-miRNAs) expression levels for several tested miRNAs were not different between control and TLE-HS samples. These findings suggest loss of Dicer and failure of mature miRNA expression may be a feature of the pathophysiology of HS in patients with TLE