摘要

Wall EH, Bond JP, McFadden TB. Acute milk yield response to frequent milking during early lactation is mediated by genes transiently regulated by milk removal. Physiol Genomics 44: 25-34, 2012. First published October 25, 2011; doi:10.1152/physiolgenomics.00027.2011.-Milking dairy cows four times daily (4x) instead of twice daily (2x) during early lactation stimulates an increase in milk yield that partly persists through late lactation; however, the mechanisms behind this response are unknown. We hypothesized that the acute mammary response to regular milkings would be transient and would involve different genes from those that may be specifically regulated in response to 4x. Nine multiparous cows were assigned at parturition to unilateral frequent milking (UFM; 2x of the left udder half, 4x of the right udder half). Mammary biopsies were obtained from both rear quarters at 5 days in milk (DIM), immediately after 4x glands had been milked (experiment 1, n = 4 cows), or 2.5 h after both udder halves had last been milked (experiment 2, n = 5 cows). Affymetrix GeneChip Bovine Genome Arrays were used to measure gene expression. We found 855 genes were differentially expressed in mammary tissue between 2x vs. 4x glands of cows in experiment 1 (false discovery rate %26lt;= 0.05), whereas none were differentially expressed in experiment 2 using the same criterion. We conclude that there is an acute transcriptional response to milk removal, but 4x milking did not elicit differential expression of unique genes. Therefore, there does not appear to be a sustained transcriptional response to 4x milking on day 5 of lactation. Using a differential expression plot of data from both experiments, as well as qRT-PCR, we identified at least two genes (chitinase 3-like-1 and low-density lipoprotein-related protein-2 that may be responsive to both milk removal and to 4x milking. Therefore, the milk yield response to 4x milking may be mediated by genes that are acutely regulated by removal of milk from the mammary gland.

  • 出版日期2012-1