Detection of allele and genotype frequencies of bovine leukocyte adhesion deficiency, factor XI deficiency and complex vertebral malformation disease genes in Holstein cattle


Cakmak N. H., Yardibi H.

ANKARA UNIVERSITESI VETERINER FAKULTESI DERGISI, cilt.66, sa.3, ss.311-315, 2019 (SCI-Expanded) identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 66 Sayı: 3
  • Basım Tarihi: 2019
  • Doi Numarası: 10.33988/auvfd.436199
  • Dergi Adı: ANKARA UNIVERSITESI VETERINER FAKULTESI DERGISI
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, TR DİZİN (ULAKBİM)
  • Sayfa Sayıları: ss.311-315
  • İstanbul Üniversitesi Adresli: Evet

Özet

Hereditary diseases cause yield and economic loses. It is important to examine hereditary diseases at the molecular level and to remove diseases from the herd. In our study, it was aimed to determine allele frequencies of genes that cause bovine leukocyte adhesion deficiency, factor XI deficiency and complex vertebral malformation diseases in Holstein cattle. Blood samples were randomly taken from 300 Holstein cattle in different dairy farms in Kocaeli, Sakarya and Balikesir provinces. Deoxyribonucleic acid samples were isolated from blood samples by using the standard ammonium acetate salt-out method. The target regions were amplified by polymerase chain reaction to determine the mutant alleles causing bovine leukocyte adhesion deficiency, factor XI deficiency and complex vertebral malformation. According to the nucleotide chromotograms of the samples subjected to bovine leukocyte adhesion deficiency analysis, it was determined that 4 out of 300 cattle were heterozygous and 296 were homozygous. Polymerase chain reaction procedure for factor XI deficiency disease was sufficient, while samples amplified by polymerase chain reaction for complex vertebral malformation disease were subjected to restriction particle length polymorphism. Factor Xl deficiency and complex vertebral malformation disease genes were all homozygous normal.