Lack of population subdivision among the minke whales (Balaenoptera acutorostrata) from Icelandic and Norwegian waters based on mitochondrial DNA sequences

The minke whale (Balaenoptera acutorostrata) is subject to commercial whaling, but stock identification and assessment are still uncertain. Mitochondrial DNA (mtDNA) sequences were determined to examine the population structure of minke whales from the central and northeastern parts of the North Atlantic, as well as the Antarctic regions IV and V. The analyses include 345 nucleotide positions of the control region of 110 individuals, and 250 nucleotide positions of the NADH dehydrogenase subunit 2 gene for a representative selection of North Atlantic minke whales. Maximum parsimony analyses and sequence divergence calculations did not reveal any genetic differentiation between individuals from the central and northeastern parts of the North Atlantic. These results do not support the International Whaling Commission's separation of minke whales in this area into different management units, and they are in conflict with previously reported results from allozyme analyses. Comparison of minke whale control region sequences showed that the sequence diversity of North Atlantic minke whales is substantially lower (0.0065) than that of Antarctic minke whales (0.0166), and clearly demonstrated that individuals from these two areas represent genetically distinct populations.     

Prenatal diagnosis of NADH:ubiquinone oxidoreductase deficiency

NADH:ubiquinone oxidoreductase (complex I of the mitochondrial respiratory chain) deficiency is a severe disorder with an often early fatal outcome. Prenatal diagnosis for complex I defects currently relies mainly on biochemical assays of complex I in fetal tissues such as chorionic villi (CV), and is only in a minority of cases possible by means of mutational analysis of nuclear-encoded genes of complex I. We report on our experience to date with prenatal diagnosis in pregnancies at risk for complex I deficiency. We measured complex I activity in native CV and/or cultured CV in 23 pregnancies in 15 families. In accordance with the results of the investigations in CV, 15 children were born clinically unaffected. Two prenatally diagnosed unaffected fetuses and two prenatally diagnosed affected fetuses were lost prematurely with spontaneous or provoked abortions, respectively. Two affected children were born (prenatally found to be affected). In two pregnancies a discrepancy between native and cultured cells was found. We conclude that prenatal diagnosis for complex I deficiency can be reliably performed. Pitfalls were encountered in using cultured CV as a result of maternal cell contamination (MCC). Future research on pathogenic nuclear mutations underlying complex I deficiency will extend the possibilities for prenatal diagnosis at the molecular level. Copyright © 2001 John Wiley & Sons, Ltd.