Tokanui Cow Lactation Research

April 2011

Understanding milk production regulation mechanisms in dairy cows

A look at one of two trials being conducted by AgResearch at Tokanui – aimed at improving productivity in diary cows by looking at cow lactation.

AgResearch’s research in dairy cow milk production focuses on looking for ways to improve production.

The aim of the research is to identify the molecular mechanisms within the mammary gland of the dairy cow which regulate milk production and to understand how these are controlled by environmental, nutritional and local cues. To achieve this they carried out several cow lactation trials at the AgResearch Tokanui dairy farm during the last lactation and current lactation seasons.

The idea is that the outcome of the trials will make their way into breeding schemes for farmers.

How do you regulate lactation performance?

In dairy cows, the ability of the mammary gland to produce milk is dependent on the number of milk secreting cells and their level of activity. Following the birth of the calf, increased secretory activity means a rise in milk production to peak levels. This is followed by a gradual decline in milk yield due to a loss in the cells which synthesize the milk. The mechanisms regulating this loss in milk yield are still unclear.

Kuljeet Singh, Senior Scientist, says they are trying to understand what is regulating milk production. Why does it peak then drop off? How do we reduce that drop off?

The development of two cow lactation models to understand the molecular mechanisms regulating milk production has been a major achievement in the research so far.

Trial 1:

To gain further understanding of the molecular mechanisms regulating the loss of milk production, the lactation persistency model was established in the 2009/10 season by selecting high and low persistency cows based on previous lactation records.

Preliminary analyses showed a good divergence in persistency in late lactation, indicating a commercially significant 5% difference in total milk yield.

Daily milk yield data, monthly blood and milk samples for composition and hormone assays were collected. Mammary biopsies at peak and late lactation were also taken.

The aim of this trial is to further AgResearch’s understanding of the critical genes regulating milk productivity.

The theory is that the proportion of active and quiescent cells is an important determinant of lactation persistency. Thus, they are currently exploring stem cell, cell proliferation and cell death signalling mechanisms.

Trial 2:

Frequent milking of dairy cows during early lactation results in an enhanced lactation performance (lactation persistency), even after cows are returned to less frequent milking.

They are currently monitoring the half udder milk yields for the remainder of lactation.

Why are they doing this? The mechanisms underlying this effect are still unclear. This response appears to be regulated locally, at the level of the mammary gland.

Whilst the immediate effect of increased milking frequency influences the cells which synthesize milk, its effects long-term may be mediated via an overall increase in MEC numbers. MEC stands for mammary epithelial cells, these are the cells in the udder that make the milk proteins.

In addition to cell signalling pathways regulating MEC number and activity, the potential of DNA methylation regulation will be explored. (DNA methylation is a mechanism that regulates the expression of genes. Therefore this is a potential mechanisms for regulating milk production).

In this trial the 20 cows in the trial mob had udder halves milked either 1x or 4x daily for two weeks during early lactation. Mammary biopsy samples were collected.

Why are they doing this? The half-udder design is extremely powerful, eliminating inter-animal variation due to environmental factors, nutrition, and genetics. In addition, both udder halves are exposed to the same systemic factors, therefore differences between udder halves can be attributed to localised effects in response to milking frequency.