Genetic merit for fertility traits in Holstein cows: III. Hepatic expression of somatotropic axis genes during pregnancy and lactation.
The objective of this study was to characterize the circulating concentrations of insulin-like growth factor-I (IGF-I) and the hepatic expression of key genes regulating the somatotropic axis in cows divergent in genetic merit for fertility traits but with similar genetic merit for milk production traits. A total of 11 cows with good genetic merit for fertility (Fert+) and 12 cows with poor genetic merit for fertility (Fert-) underwent liver biopsy by percutaneous punch technique on d 20 (±6.7 d) prepartum and on d 2 (±1.5 d), d 58 (±3.7 d), d 145 (±13 d), and d 245 (±17.1 d) postpartum. Total RNA was isolated and the mRNA expression of growth hormone receptor (GHR 1A and GHRtot), IGF-I, janus tyrosine kinase 2 (JAK2), signal transducer and activator of transcription 5B (STAT5B), suppressor of cytokine signaling 3 (SOCS-3), acid-labile subunit (ALS), and IGF-binding proteins (IGFBP1 to IGFBP6) were measured by real-time quantitative PCR. During lactation, the circulating concentrations of IGF-I were 34% greater in Fert+ cows. The Fert+ cows had increased mean expression of IGF-I mRNA during the study; however, the difference in IGF-I mRNA abundance between Fert+ and Fert- cows was most pronounced at d 145 and 245. The expression of IGFBP3 and ALS transcript was similar in Fert+ and Fert- cows for the duration of the study. The Fert- cows, however, had greater expression of IGFBP2, IGFBP4, IGFBP5, and IGFBP6. Genotype had no effect on mRNA abundance of GHR 1A, STAT5B, JAK2, or SOCS-3. Genetic merit for fertility traits affects hepatic expression of key genes of the somatotropic axis regulating the synthesis, bioavailability, and stability of circulating IGF-I.
Animal and Grassland Research and Innovation Centre, Teagasc, Moorepark, Fermoy, Co. Cork, Ireland.
S B
SB
Cummins
S M
SM
Waters
A C O
AC
Evans
P
P
Lonergan
S T
ST
Butler
D000818:Animals; D002352:Carrier Proteins / Q000032:analysis / Q000235:genetics; D002417:Cattle / Q000235:genetics* / Q000502:physiology; D005260:Female; D005298:Fertility / Q000235:genetics* / Q000502:physiology; D005796:Genes / Q000235:genetics / Q000502:physiology; D006023:Glycoproteins / Q000032:analysis / Q000235:genetics; D018969:Insulin-Like Growth Factor Binding Proteins / Q000032:analysis / Q000235:genetics; D007334:Insulin-Like Growth Factor I / Q000032:analysis; D053614:Janus Kinase 2 / Q000032:analysis / Q000235:genetics; D007774:Lactation / Q000235:genetics* / Q000502:physiology; D008099:Liver / Q000737:chemistry / Q000378:metabolism*; D011247:Pregnancy; D011270:Pregnancy, Animal / Q000235:genetics* / Q000502:physiology; D019655:Quantitative Trait, Heritable; D011986:Receptors, Somatotropin / Q000032:analysis / Q000235:genetics; D050799:STAT5 Transcription Factor / Q000032:analysis / Q000235:genetics; D050826:Suppressor of Cytokine Signaling Proteins / Q000032:analysis / Q000235:genetics
D002352:Carrier Proteins; D006023:Glycoproteins; D018969:Insulin-Like Growth Factor Binding Proteins; D011986:Receptors, Somatotropin; D050799:STAT5 Transcription Factor; D050826:Suppressor of Cytokine Signaling Proteins; C075944:insulin-like growth factor binding protein, acid labile subunit; D007334:Insulin-Like Growth Factor I; D053614:Janus Kinase 2