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Scientists Develop First Transgenic Cow Clone for Mastitis Disease ResistanceBy Jan Suszkiw
January 10, 2001
BELTSVILLE, Md., Jan. 10--U.S. Department of Agriculture and University of Vermont (UV) researchers have produced a clone of a pure-bred Jersey cow whose cells may offer a biotechnological defense against mastitis disease.
Geneticist Kevin Wells of USDAs Agricultural Research Service (ARS) said it will be at least another year before the cow, named Annie and born in March 2000, begins producing milk and scientists can begin testing for mastitis resistance. Though not the first cow clone, Annie is the first to be genetically altered with a gene for an agricultural application.
Mastitis costs U.S. dairy farmers about $1.7 billion annually, including lost milk revenues, said Wells, with ARS Gene Evaluation and Mapping Laboratory at Beltsville.
About 30 percent of all mastitis cases in dairy cows are caused by Staphylococcus aureus bacteria that destroy milk-secreting cells in the animals mammary gland. But scientists hope that Annie will resist such cellular attacks by secreting an added protein called lysostaphin.
Antibiotics are only effective in about 15 percent of cows infected with S. aureus, so dairy producers are forced to cull these cows from their herds. But lysostaphin may offer an alternative defense bioengineered right into the animals cells.
Were also trying to identify naturally occurring resistance genes, though very few of them have been found, noted Vernon Pursel, the GEMLs research leader. Whether bioengineered or naturally occurring, he said, resistance would lessen mastitiss financial drain, and provide the added public health benefit of reduced antibiotic usage.
In 1999 trials with seven transgenic strains of lysostaphin-producing mice, the protein effectively killed S. aureus bacteria in both the genetically modified rodents mammary glands and milk, GEML physiologist Robert Wall said. He and David Kerr of UVs Animal Sciences Department in Burlington, report the results in January 2001 issue of the journal Nature Biotechnology.
S. aureus was targeted by scientists because it is among the most virulent of mastitis causing pathogens, and causes about 30 percent of all infections in cows. The gene for lysostaphin--interestingly--comes from a benign species of Staph--S. simulans--that competes with its virulent cousins.
Large-scale testing of lysostaphin mice in the lab will help researchers learn whether results observed in these transgenic rodents will apply to Annie and her offspring. Practical application of the cloning technology is several years off, however, Pursel said. First, a number of questions must be thoroughly researched. For example:
Another objective is to refine the cloning procedure scientists used, called somatic cell nuclear transfer. Annies start began with a type of somatic cell called a fibroblast. Using a mild electrical current, scientists inserted into that fibroblasts nucleus, genes for lysostaphin, a green fluorescent protein (GFP) tag, and an antibiotic marker. Also inserted was a sheep gene for beta lactoglobulin, a switch that instructs mammary cells to make lysostaphin.
Later, scientists fused the altered fibroblast to an unfertilized cow egg, whose nuclear DNA contents had been removed so the fibroblasts could move in. About 60 percent of fused cells actually survive, and start dividing like a normal fertilized embryo, said Pursel. The healthiest embryos--which included Annie--were cultured and implanted into surrogate mothers.
So far, Annie is the first calf brought to term. Genetic testing of umbilical cord tissue at birth confirmed that she is indeed transgenic. Annie Powell--for whom the Jersey clone is named--Paul Graninger, Neil Talbot, Harold Hawk, and Linda Mooney are the other ARS contributing team members.
Scientific contacts: Kevin Wells or Robert Wall, ARS Gene Evaluation and Mapping Laboratory, Beltsville, Md., phone (301) 504-8342, fax (301) 504-8414, email@example.com, firstname.lastname@example.org.