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Submitted on January 22, 2002
Accepted on July 30, 2003
1 USDA/ARS Children's Nutrition Research Center. Department of Pediatrics and Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston TX. 77030. Department of Pharmacology, The Pennsylvania State University, The Milton S. Hershey Medical Center, Hershey PA., Department of Obstetrics and Gynecology, University of Texas Medical Branch, Galveston, TX. Harbor-UCLA Medical Center, Torrance CA., Department of Molecular Genetics, The University of Texas M. D. Anderson Cancer Center, Houston TX.
* To whom correspondence should be addressed. E-mail: dhadsell{at}mbcr.bcm.tmc.edu.
Previous studies have suggested upstream stimulatory factors (USF) regulate genes involved with cell cycle progression. Because of the relationship of USFs to an important oncogene in breast cancer, c-myc, we chose to determine the importance of USF to normal mammary gland development in the mouse. Expression of USF in the mammary gland throughout development demonstrated only modest changes. Mutation of the Usf2 gene was associated with reduced fertility in females, but had no effect on prepartum mammary gland development. However, lactation performance in Usf2-/- females was only half of that observed in Usf2+/+ females and both lactose and nitrogen were decreased in milk from Usf2-/- dams. This decrease was associated with diminished mammary tissue wet weight, and luminal area by day 9 of lactation and with a decreased in protein:DNA ratio. This decrease was associated with reduced abundance of the translation initiation factors eIF4e and eIF4g. Blood oxytocin concentrations on day 9 postpartum were also lower in Usf2-/- mice than Usf2+/+ mice. In contrast, the mutation had no effect on blood PRL concentrations, mammary cell proliferation or apoptosis, mammary tissue oxytocin receptors, or milk protein gene expression. The mutation had only modest effects on maternal behavior. These data support the idea USF is important to physiological processes necessary for the establishment and maintenance of normal lactation and suggests that USF-2 may impact lactation through both systemic and mammary cell-specific mechanisms.
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