AGRONOMIJAS VĒSTIS - Latvijas Lauksaimniecības universitāte

AGRONOMIJAS VĒSTIS (Latvian Journal of Agronomy), No.10, LLU, 2008The comparison of sequence results of the both allele 1 and allele 2 (Fig. 2A and B)allowed us to read the sequences we have obtained for resting three animals (Fig. 2C) and to makeconclusion on heterozygote genotype of gene portion analyzed (Table 1, Fig. 2).Based on the analysis of both homozygote and heterozygote conditions of allele 2 wesuggest that SNP A 766 →T could be linked with MS motif in one linkage block.In our pilot study we demonstrated that MSTN gene MS polymorphism is represented inLatvian Blue cattle breed at least by two alleles of different repeated portion motifs andneighbouring SNPs polymorphisms. In set of 7 animals analyzed allele 1 was more frequent (6 and3 alleles for 3 homozygotes and 3 heterozygotes correspondingly) and allele 2 was revealed as lessfrequent ( 2 and 3 alleles for 1 homozygote and 3 heterozygotes). As animals were not selectedspecially for any traits we could suggest that the same allele presentation and distribution couldcharacterize Latvian Blue cattle breed in general. However, broad population study is necessary toprove all our suggestions.ConclusionsMSTN gene MS polymorphism is represented in Latvian Blue cattle breed at least by twoalleles of different repeated portion motifs and neighbouring SNPs polymorphisms.Allele 2 is different from the reported sequence (GeneBank: AB076403) variant not only inMS core motif but also in several SNPs including SNP A 766 →T in 5’ region from the MS repeatedportion.Longest allele 1 was more frequent and shortest allele 2 was revealed as less frequent. Asanimals were not selected specially for any traits we could suggest that the same allele presentationand distribution could characterize Latvian Blue cattle breed in general.AcknowledgementsAuthors are grateful to Latvian Ministry of Agriculture for financial support, contractworks No 120706/S386 and No 201006/C-266. We thank Ilva Poudziunas for assistance.References1. Charlier, C., Coppiters, W., Farnir, F., Grobet, L., Leroy, P., Michaux, C., Mni, M., Schwers, A.,Vanmanshoven, P., Hanset, R. (1995) The mh gene causing double muscling in cattle maps to bovinechromosome 2. Mamm. Genome 6, 788-792;2. De la Rosa-Reyna, X. F., Perez, M. A. R., Sifuentes-Rincon, A. M. (2005) Microsattelite polymorphismin intron 1 of the bovine myostatin gene. J. Appl. Genet., 47, 1–3;3. Grislis, Z. (2006). Zilās Govs Vidzemē. Biedrība Širnes saglabāšanas apvienība “Zilā Govs”. Jelgava,36.4. Grobet, L., Martin, L., Poncelet, D., Pirottin, D., Brouwers, B., Riquet, J., Schoeberlein, A., Dunner, S.,Mienissier, J., Joulia-Ekaza, D., Cabello, G. (2006) Myostatin regulation of muscle development: Molecularbasis natural mutations, physiopathological aspects. Exp. cell research 312,2401-2414;5. Kambadur, R., Sharma, M., Smith, T. P., Bass, J. J. (1997) Mutations in myostatin (GDF8) in doublemuscledBelgian Blue and Piedmontese cattle. Genome Res. 7, 910-916;6. Karim, L., Coppieters, W., Grobet, L., Valentini, A., Georges, M. (2000) Convenient genotyping of sixmyostatin mutations causinf double-muscling in cattle a multiplex oligonucleotide ligation assay.Anim.Genet. 31, 396-399;7. Kassar-Duchaaussoy, L., Gayraud-Morel, B., Gomes, D., Rocancourt, D., Buckingham, M., Shinin, V.,Tajbakhsh, S. (2004) Mrf4 determines skeletal muscle identity in Myf5: MyoD double-mutant mice. Nature431, 466-471;8. Lewin, B. (2004) Genes VΙΙΙ.Pearson,Prentice Hall.9. McPherron, A., Lee, S. (1997) Double muscling in cattle due to mutations in the myostatin gene.Proceeding of the National Academy of Science of the United States of America, 94, 12457–12461;10. Rudnicki, M., Braun, T., Hinuma, S., Jaenisch, R. (1992) Inactivation of MyoD in mice leads to upregulationof the myogenic HLH gene Myf-5 and results in apparently normal muscle development. Cell 71,383-390;11. Sjakste, T., Zhuk, A. (2006) Novel haplotype description and structural background of the eventualfunctional significance of the barley beta-amylase gene intron rearrangements. Theor.Appl.Genet. 113, 1063-1079;270