Analysis of lactation defects in transgenic mice.

Although lactation is the only physiological function of the mammary gland, little is known about the molecular events required for secretory activation and milk production. Genetically altered mice have been used extensively to study mammary gland development during puberty and pregnancy, as well as mammary tumorigenesis. A number of approaches have been used to produce genetic modifications in mammary glands of mice, including transgenic mice utilizing mammary specific promoters, traditional knockout mice, mammary-specific gene deletion, and conditionally-regulated transgenes.

Metabolic regulation in the lactating mammary gland: a lipid synthesizing machine.

The mammary gland of the lactating mouse synthesizes and secretes milk lipid equivalent to its entire body weight in a single 20-day lactation cycle, making it one of the most active lipid synthetic organs known. We test the hypothesis that multiple control points and potential regulatory mechanisms regulate milk lipid synthesis at the level of gene expression. The mammary transcriptome of 130 genes involved in glucose metabolism was examined at late pregnancy and early lactation, utilizing data obtained from microarray analysis of mammary glands from quadruplicate FVB mice at pregnancy day 17 and lactation day 2.

Calcium secretion into milk.

Ionized calcium ([Ca(2+)]) is present in milk at concentrations around 3 mM, a concentration that drives the formation of complexes with citrate, phosphate, and casein, thereby generating compounds that carry the major portion of calcium in milk. In humans and cows, where it has been studied, changes in milk calcium appear to be regulated by the amount of citrate and casein in milk rather than changes in [Ca(2+)]. Most or all of the calcium in milk is likely derived through exocytosis of secretory vesicles derived from the Golgi compartment where a calcium ATPase mediates transport from the cytoplasm.

Characterization of fluorescent chimeras of cholera toxin and Escherichia coli heat-labile enterotoxins produced by use of the twin arginine translocation system.

Cholera toxin (CT) is an AB(5) toxin responsible for the profuse secretory diarrhea resulting from Vibrio cholerae infection. CT consists of a pentameric, receptor-binding B subunit (CTB) and a monomeric A subunit (CTA) that has latent enzymatic activity. In addition to its enterotoxicity, CT has potent mucosal adjuvant activity and can also function as a carrier molecule with many potential applications in cell biology.