Autumn microhabitat breadth differs between family groups of Atlantic salmon parr (Salmo salar) in a small chalk stream

The effect of family traits on the microhabitat use by six genetically distinct groups (three in each year of study) of juvenile Atlantic salmon tagged with passive integrated transponder (PIT) tags was studied via PIT-tag detectors installed on the river bed in a small chalk stream of southern England, during Autumn in 2006 and 2007. Canonical correspondence analysis of the molecular and microhabitat data revealed considerable overlap in the microhabitat use of the family groups and notable differences in microhabitat breadth, which was partly influenced by sample size. The data suggest that microhabitat breadth and preferences of wild salmon are influenced by family of origin

Glycine decarboxylase deficiency causes neural tube defects and features of non-ketotic hyperglycinemia in mice.

Glycine decarboxylase (GLDC) acts in the glycine cleavage system to decarboxylate glycine and transfer a one-carbon unit into folate one-carbon metabolism. GLDC mutations cause a rare recessive disease non-ketotic hyperglycinemia (NKH). Mutations have also been identified in patients with neural tube defects (NTDs); however, the relationship between NKH and NTDs is unclear. We show that reduced expression of Gldc in mice suppresses glycine cleavage system activity and causes two distinct disease phenotypes. Mutant embryos develop partially penetrant NTDs while surviving mice exhibit post-natal features of NKH including glycine accumulation, early lethality and hydrocephalus. In addition to elevated glycine, Gldc disruption also results in abnormal tissue folate profiles, with depletion of one-carbon-carrying folates, as well as growth retardation and reduced cellular proliferation. Formate treatment normalizes the folate profile, restores embryonic growth and prevents NTDs, suggesting that Gldc deficiency causes NTDs through limiting supply of one-carbon units from mitochondrial folate metabolism