With next-generation sequencing, DNA sequences of a community of aquatic vertebrates could be analyzed simultaneously, exponentially increasing the data available for analysis without disturbing sensitive species. Other applications include early detection of invasive species, determining whether invasive species have been successfully removed through management actions, detecting rare individuals surviving after catastrophic population declines, and discovering new species in rapid bioassessement surveys. Sensitivity of these techniques to density of individuals and covariates of detection probability such as water temperature and discharge will need to be determined for study systems individually; however, this technique shows great potential for increasing our knowledge of aquatic systems. Mutations in Leucine Rich Repeat Kinase 2 are the most common Mendelian genetic cause of Parkinson��s disease currently identified. Additionally, variation at this locus has high levels infection recently been implicated as a risk factor for sporadic PD in two genome wide association studies. Although the function of LRRK2 is unknown, the presence of a kinase domain, a GTPase domain and protein/protein interaction domains within its open reading frame has led to suggestions that it could act as a signaling node within cells, with the protein/protein interaction regions functioning as scaffolding areas to recruit binding partners and substrates to an active complex. LRRK2 has been implicated in a number of signaling pathways including ERK signaling and the mTOR pathway. It is likely that if LRRK2 does act in this manner, then alterations in the activity of this protein would result in changes in signaling pathways leading to downstream shifts in gene expression. In addition, a recent study has suggested that pathogenic forms of LRRK2 bind directly to the miRNA processing enzyme Argonaute and thus influence mRNA levels in a Drosophila model of LRRK2 disease. Because mammalian miRNAs potently reduce mRNA levels, the prediction from the Drosophila data would be that steady state mRNA levels of miRNA targets are altered in the presence of mutant LRRK2. To test whether mutations in LRRK2 cause an alteration in basal gene expression we have examined the impact of mutations in three contexts: fibroblast cells cultured from PD patients carrying mutations in LRRK2, brain tissue from 5 patients carrying the G2019S mutation compared to idiopathic PD and control brain tissue, and HEK293T cells stably transfected with a plasmid allowing inducible expression of LRRK2 with or without the R1441C mutation. We have compared global gene expression in these systems, searching for differences between wild type and mutant conditions. This study assessed a series of patient fibroblast cells harbouring mutations in LRRK2, brain samples from G2019S carriers and a cell line system over-expressing LRRK2 wild type and mutant transgenes for alterations in gene expression due to the presence of mutant LRRK2. Overall, our data show that any differences in gene expression are lower than the relatively modest cutoffs used. In turn, this suggests that mutant LRRK2 does not elicit large changes in steady state mRNA levels within the cell under normal growth conditions. This is in contrast to a recent publication studying a series of mononuclear cells carrying the G2019S mutation and data from Drosophila and a HEK cell model. There are a number of possible reasons for the divergence in our data from those in these studies.