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They focused on editing specific imprinting control regions (ICRs), sequences of DNA that act as gene control switches.
The standard mix of male and female genes provides a healthy balance of ICR coding – but if only mom or dad genes are used, this coding goes haywire.
Researchers have successfully bred a mouse (right) that has two male parents (one pictured left) and can survive to adulthood by editing their genes to overcome developmental challenges
In order to breed offspring which have two biological fathers, the researchers first needed to transform the male sex cells from one parent into female sex cells.
The scientists took sperm from a mouse and injected it into a type of cell called an oocyte - an immature egg cell that has had its genetic material removed in a process called enucleation.
This created a stem cell - a type of cell with the potential to become any other type of cell in the body - which contained only male DNA from the first parent.
The researchers then took one of these stem cells and a sperm cell from another male and injected both into another enucleated immature egg.
These male cells combined to create an embryonic stem cell containing the DNA of both parents, which was then used to create an embryo which could be implanted in a surrogate mother.
Once the embryo had developed, the mother gave birth to the offspring, which contained only genetic material from the two males.
Scientists have known for a long time that this is possible and have managed to create viable embryos using the technique.
However, no one has previously managed to create 'bi-paternal' mice that are actually capable of surviving to adulthood.
By changing genes which control how the parents' chromosomes combine, the bi-paternal mice lived much longer and could even survive weaning.
Most of the adults had a short lifespan, and all the adult mice ended up sterile. In the new study, published Tuesday (Jan. That the researchers were able to get it to work with two fathers adds to the importance of the study.
Now we shouldn't get ahead of ourselves: this is still a very difficult process in mice, which fails a lot of the time, and it's going to be a long while before scientists can think about whether the same techniques could be used for human embryos.
Even then, there will be a host of ethical and philosophical questions to address, but eventually this research could drive improvements in fertility treatments and our understanding of congenital disorders.
"Although the efficiency is low at present, this finding may be an important step toward achieving mammalian androgenesis," write the researchers.
The research has been published in PNAS.
That might not sound like a particularly impressive success rate, but it's above zero – and the two survivors then went on to reproduce normally and have healthy mouse pups.
While there's obviously lots of room for improvement in terms of how many mice are born and live to see adulthood, and how exact the ICR editing techniques can be, it shows that this approach to imprint editing can work.
This is something that's easier to do when there are two mothers involved, by the way: the edits required are fewer and easier to carry out.
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By contrast, the handful of mice that were bred in Japan and survived to adulthood were fertile.
"Our next steps include refining the gene editing approach to produce healthier bi-paternal animals," Li said. But this is just a start in what could be a game-changer in not just refining unisexual reproduction, but understanding imprinting’s role in many human diseases.
“These findings provide strong evidence that imprinting abnormalities are the main barrier to mammalian unisexual reproduction,” said coauthor Guan-Zheng Luo of Sun Yat-sen University in Guangzhou in the statement.
Kotaro Sasaki, an associate professor in the University of Pennsylvania School of Veterinary Medicine and Perelman School of Medicine who was not involved in the work.
Related: CRISPR 'will provide cures for genetic diseases that were incurable before,' says renowned biochemist Virginijus Šikšnys
However, the resulting mice still had deficits, including shorter lifespans than normal mice, Sasaki told Live Science in an email.
The mice had abnormalities, such as umbilical hernias, protruding tongues and enlarged internal organs.
Systematically, the researchers pinpointed the genetic origin of each of these issues and introduced more and more genetic tweaks to the mice. Simply put, it causes too many genes to go haywire.
To address this, the researchers first grew stem cells from sperm DNA.
They then edited the stem cells to prevent twenty mice genes known to be heavily involved in their developmental stage from being imprinted.
While it’s just a portion of the total number that undergo this process in mice, according to MIT Technology Review, it made an impact. Your details from Facebook will be used to provide you with tailored content, marketing and ads in line with our Privacy Policy.