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Structural characteristics and polymorphism of the long (LNR) and short (SNR) mitochondrial noncoding regions were studied in the liver fluke Fasciola hepatica. Flukes were sampled from several populations of Russia and Belarus. LNR amplification yielded a set of nine fragments, neighboring ones differing in length by one tandem repeat (85 bp), published for Australian flukes. The LNR amplification products of different lengths were cloned and sequenced. A comparison of the LNR sequences of Australian and Belarussian flukes revealed three nucleotide substitutions and one point heteroplasmy in the first positions of the imperfect repeat and four adjacent perfect repeats. The positions of the three mutations coincided in the perfect and imperfect repeats. The frequency of mutations was 4.0–4.7 %, while the frequency of heteroplasmic sites varied from 0.1 to 1.2%. It was shown that the mutations and the heteroplasmy of one site could change the structure and stability of the putative secondary structures of the perfect and imperfect repeats. SNR amplification in F. hepatica from several populations yielded fragments that differed from the published SNR sequence of Australian F. hepatica by one transversion (T → G in position 21). Both noncoding regions had several conserved and potential regulatory sequences. The possible causes of heteroplasmy and a concerted origin of substitutions in different repeats are discussed.

Structural characteristics and polymorphism of long (LNR) and short (SNR) mitochondrial non-coding regions of the liver fluke Fasciola hepatica were studied. The flukes were obtained from several populations of Russia and Belarus. The amplification of LNR yielded a set of 10 fragments with the length of neighbouring ones differing in one tandem repeat (85 bp; published earlier for Australian fluke). LNR amplification fragments of different length were cloned and sequenced. Comparison of the LNR sequences of Australian and Belarussian flukes revealed 3 nucleotide substitutions and one point heteroplasmy of the first nucleotides in the imperfect repeat and four adjacent perfect repeats. Positions of the three mutations coincide in perfect and imperfect repeats and the frequency of mutations is 4-4.7% while the frequency of heteroplasmic sites varies from 0.1 to 1.2%. It was shown that the presence of mutations and the heteroplasmy of one site can change the structure and stability of the putative secondary structures of the perfect and imperfect re- peats. The amplification of SNR of F. hepatica from several populations yielded fragments which differed from the published SNR sequence of Australian F. hepatica in the single transversion. Both non-coding regions have several conservative and potentially regulatory sequences. Probable cause of heteroplasmy and concerted origin of substitutions in different repeats are discussed.