Israeli scientists have demonstrated the ability for mammals to mate and produce only female babies. A similar system based on identical principles could produce only males.
The research for the study was led by Prof. Udi Qimron, Dr. Ido Yosef and Dr. Motti Gerlic and conducted by Dr. Liat Edry-Botzer, Rea Globus, Inbar Shlomovitz and Prof. Ariel Munitz, all of the Department of Clinical Microbiology and Immunology at Tel Aviv University's Sackler School of Medicine. The research was published in EMBO Reports.
"We proved the concept in mouse models, but the concept could also be demonstrated in cattle, swine, goats, chickens and other animals," Qimron said. He noted that humans are likewise mammals and the concept could ultimately be applied to human children "if a mad ruler decides he wants to engineer the people to have only male or female offspring - we have provided the proof of concept."
Last year, in what became a ground-breaking and controversial medical first, a scientist in China claimed to have created the world's first genetically edited babies. The researcher, He Jiankui of Southern University of Science and Technology in Shenzhen, said he altered embryos for seven couples during fertility treatments, with one pregnancy resulting so far. He said his goal was not to cure or prevent an inherited disease, but to try to bestow a trait that few people naturally have: an ability to resist possible future infection with HIV.
This kind of gene editing is banned in most countries.
But the researchers at TAU worked differently and, according to Qimron, have a different agenda. The researchers crossed two types of genetically engineered mice. The maternal mouse encoded a Cas9 protein, a CRISPR-protein that is inactive unless guided by special "guide-RNAs." The paternal mouse encoded these guide-RNAs on the Y-sex chromosome, a sex chromosome present only in males. After fertilization, the guide-RNAs from the paternal sperm and the Cas9 protein from the maternal egg were combined in the male mouse embryos, but not in the female embryos (because the females lack the Y chromosome). The combination of guide-RNAs with Cas9 results in a complex that eliminates the male embryos.
"We showed that Cas9 was specifically activated only in male embryos," said Qimron. "Our results pave the way for a genetic system that allows biased sex production. When two transgenic types of mice encoding Cas9 or Y-chromosome-encoded guide-RNAs are crossed, lethality of males occurs because Cas9 is guided from the Y chromosome to target essential genes. This does not happen in females because the Y chromosome is not transferred to them. This cross thus halts embryonic development of males without affecting the development of females."
The idea for the research came after one of Qimron's research fellows, Yosef, saw an advertisement stating that billions of chickens were killed annually by chicken egg farmers who had no use for so many male chicks.
"He said, 'There must be a way to overcome this,'" Qimron recalled. "It is so cruel and unfair and we thought there must be a scientific solution."
The team started with mice, but Qimron said he believes the same system could transfer to other animals and species of animals, including cattle.
This could save the lives of thousands of cows who are killed each year on dairy or meat farms.
The number of male calves being killed straight after birth is high on dairy farms because it is cheaper to kill them than to rear them, for example. And on beef farms, the opposite is true, where female cows are killed in favor of hefty male cattle.
The researchers based the system on one that already exists for certain plants, insects, crustaceans and fish that possess the uncanny ability to change the sex of their offspring before they are born. Mammals, however, have never before demonstrated this genetic skill, until now.
"We approached this problem in an innovative way, using genetic engineering," Qimron said. "We believe that the producers of cattle, swine and chicken may benefit greatly from the technology."
Return to News Home
