Scientists discover the gene responsible for head regrowth

Although the hydra may only be known as a Greek myth, head regrowth is actually not as fantastical as it may seem.

According Greek mythology, the hydra was a nine-headed serpent slain by Hercules. What made the feat challenging was that every time Hercules cut off one of the serpent’s heads, two new heads replaced it.

In 2008, researchers Peter Reddien and Christian Petersen of the Whitehead Institute for Biomedical Research identified the gene responsible for head regrowth: Smed-βcatenin-1.1 To investigate genes’ effects on head and tail amputation, the scientists used RNA interference to “turn off” planarian flatworms’ genes one by one. When a flatworm’s genes are left unimpeded, the worm will regenerate a tail if its tail is amputated and a head if its head is amputated. When they turned off the Smed-βcatenin-1 gene, however, Reddien and Petersen discovered that a flatworm will regenerate a head at any amputation site. In fact, if the scientists made six incisions in the side of the worm’s body, the worm would regrow six new heads.

Using the same process of RNA interference, Alejandro Sanchez Alvarado and colleagues at the University of Utah demonstrated the converse effect: they could force planarian flatworms to regrow tails at every amputation or incision site by restricting expression of the βcatenin antagonist adenomatous polyposis coli. 2

Building upon these discoveries, University of Nottingham scientist Aziz Aboobaker identified the smed-prep gene3—a gene that directs flatworms to regenerate new muscle, gastro, and even brain cells from stem cells. Moreover, the smed-prep gene targets these cells to their proper locations in the worm and organizes them into functional structures (as opposed to masses of useless cells).

The human implications of this research are enticing. Engineering a person’s body to replace damaged or diseased cells, tissues, organs, or even limbs is one possibility. This would be helpful for treating diseases such as Alzheimer’s. Also, understanding normal cell regeneration is one step toward discovering what happens when stem cells malfunction during the process of cell renewal, which occurs in diseases such as leukaemia.

Watch 8-headed planarian regeneration from Peter Reddien’s lab:

1 Petersen, C., & Reddien, P. (2008). Smed- catenin-1 Is Required for Anteroposterior Blastema Polarity in Planarian Regeneration Science, 319 (5861), 327-330 DOI: 10.1126/science.1149943

2 Gurley, K., Rink, J., & Alvarado, A. (2008). -Catenin Defines Head Versus Tail Identity During Planarian Regeneration and Homeostasis Science, 319 (5861), 323-327 DOI: 10.1126/science.1150029

3 Felix DA, & Aboobaker AA (2010). The TALE class homeobox gene Smed-prep defines the anterior compartment for head regeneration. PLoS genetics, 6 (4) PMID: 20422023

Three-Parent Babies to Prevent Mitochondrial Diseases

The research started with monkeys. In August 2009, scientists from the Oregon National Primate Research Center published a study1 in which they transplanted the DNA of monkeys with damaged mitochondria into “chromosome-empty” eggs of monkeys with healthy mitochondria. Fifteen viable embryos resulted, four of which were brought to term. The purpose of this research was to prevent conditions such as blindness, deafness, dementia, or diabetes, all of which can be caused by faulty mitochondria and affect one in every 6,500 children.

Recently, Doug Turnbull and other researchers from Newcastle University took the primate research a step further by merging fertilized human eggs—thus creating the potential for babies with three parents.2 The researchers essentially replicated the earlier study’s method, taking the DNA, or pronuclei, from the embryo created by the mother’s egg and father’s sperm and injecting it into a “hollowed out” egg belonging to a second woman (i.e. an egg from which the pronuclei have been removed). This creates an embryo with healthy mitochondria (from the donated embryo) while preserving the parental DNA (from the pronuclei).

Ethical concerns aside, several questions remain:

  • What might be the effects of having two biological mothers?
  • Could the tiny amount of damaged mitochondrial DNA that ends up in the healthy host egg still be enough to cause mitochondrial disease?

Still, researchers are optimistic that their technique will be fine-tuned and ready to undergo the ethical gauntlet in as little as three years time.

Check out another 2009 study3 in which researchers attempt to improve IVF for older women by implanting their nuclei, containing the majority of the DNA for the baby, into the healthy cytoplasm of younger donor mothers’ eggs.

1 Tachibana, M., Sparman, M., Sritanaudomchai, H., Ma, H., Clepper, L., Woodward, J., Li, Y., Ramsey, C., Kolotushkina, O., & Mitalipov, S. (2009). Mitochondrial gene replacement in primate offspring and embryonic stem cells Nature, 461 (7262), 367-372 DOI: 10.1038/nature08368

2 Craven, L., Tuppen, H., Greggains, G., Harbottle, S., Murphy, J., Cree, L., Murdoch, A., Chinnery, P., Taylor, R., Lightowlers, R., Herbert, M., & Turnbull, D. (2010). Pronuclear transfer in human embryos to prevent transmission of mitochondrial DNA disease Nature DOI: 10.1038/nature08958

3 TANAKA, A. (2009). Metaphase II karyoplast transfer from human in-vitro matured oocytes to enuclueated mature oocytes Reproductive BioMedicine Online, 19 (4), 514-520 DOI: 10.1016/j.rbmo.2009.06.004