The classic drosophila genetics experiment to cross white-eyed flies to wild-type red eyed flies to

The classic drosophila genetics experiment to cross white-eyed flies to wild-type red eyed flies to create an F1 hybrid and so on. An excellent genetics lesson as it provides a good example with which you can assess the impact of a trait that depends on a single gene. With the parental cross all were red eyed, and in the F1 back cross with white eyed parental-type there were due to be four colours (red eyes, bright red eyes, brown and white eyes). However, at some stage between the parental cross, and F1 back cross, I remember we managed to produce a one eyed white mutant drosophila that was not listed at all. My lecturer was not impressed. I considered at that point that an inabilityMcTernan BMC Obesity 2014, 1:3 http://www.biomedcentral.com/2052-9538/1/Page 3 ofto master drosophila would present significant challenges if I ever considered embarking on trying to understand the complexity of human genetics. However, despite this I feel that monogenic human obesity has shown us the extreme phenotypes (which are rare when compared to the more common form of obesity), and these offer a unique insight into obesity as a whole. Studies in mice show that these phenotypes highlight that even in these cases humans are not a simple species. Polygenic obesity by its nature has been a difficult case to crack in terms of locating those genes that appear to raise their head PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/28154141 above the significance line. Polygenic obesity association studies assessing single nucleotide polymorphisms (SNPs) have noted that many lie within the first intron of the fat mass?and obesity-associated gene (FTO) which is strongly associated with adiposity. In the initial stages before we knew that FTO encoded for a 2-oxoglutarate (2-OG) Fe2+-dependent dioxygenase, FTO showed us a revitalising glimpse of how relevant genetic studies are – despite the large scale heterogenic complexity of humans. However, it’s clear that understanding the functionality aligned with these genes, challenging though it may be, is vital for continuing studies. Whilst we know that genes affect our body fat we also now realize that the naive view that adipose tissue is just a simple storage organ has certainly gone. The molecular biology biomarker era and the more recent epigenetic studies that have been conducted have certainly given us food for thought on our way to discovering individual risk profiles. Yet significant new research programmes have decided we should also consider more closely what food we eat, and look at moving towards eating more `superfoods’, i.e. using functional food value as a potential diet related treatment option to reduce the obesity mediated metabolic risk for ourselves and offspring. It must seem like a return to AG-221 chemical information previous times, to understand the benefits that food in an unprocessed manner may have had on us and our children, having realised that previous generations were healthier than current and future ones will be. This doesn’t mean to say this avenue will be easy, as diets, gut flora and cellular metabolism thrown together may present quite a challenge to embark on even in this time of modern technologies.makes you wonder how varied all our gut floras may be. Now for example throw people onto a plane in a confined space for several hours from different countries, different homes, and different diets, then you could have up to 10,000 different species being passed around changing the species diversity and bacterial species proportion in your gut. Not of course forgetti.