The recent successful birth of twin healthy monkeys through a new gene therapy known as spindle transfer has provided hope in preventing a chain of inherited diseases which are passed from mothers to their offspring through mutated DNA in the mother’s cell mitochondria (Paddock 2009). Although uncommonly known, the mitochondria like the cell nucleus contain their own genome which is derived predominantly from the egg. Therefore, with each individual cell harboring numerous mitochondria, mutations in this DNA can occur at higher rate than nuclear DNA, resulting in 150 known diseases such as Parkinson’s disease which can be passed on to the embryo (Tachibana et al. 2009).
The fertility method, spindle transfer prevents this inheritance of mutated mitochondrial DNA through the transfer of intact spindle-chromosomal complexes [of the metaphase II stage] into a healthy donor egg containing only of healthy mitochondrial DNA. In this case, the researchers of Oregon Heath and Science University’s Oregon National Primate Research center then tested the result of this experiment in monkeys. The resumption of meiosis in the new egg was first activated through electrofusion pulse before it was fertilized by the addition of male sperm (Tachibana et al. 2009). When it was developed into an embryo, it was then implanted in female surrogate monkeys where twin monkeys, “Mito” and “Tracker” were born (Paddock 2009).
At first it was feared by these US researchers that significant mitochondrial DNA would still be able to crossover when transferred to the donor egg, however previous investigations into the distribution of mitochondria in mature Metaphase II stage oocytes has shown that spindles and metaphase chromosomes were devoid of mitochondria. Instead, the mitochondria were found to be safely suspended uniformly throughout the cytoplasm. The other obstacle involving the safe isolation of spindle-chromosomal complex was also found to be negligible through the help of a new non-invasive microscopy which avoids ultraviolet exposure and Hoechst staining damage on cell replication (Tachibana et al. 2009).
Despite the fact that there are some subtle differences between monkeys and humans in general, it is believed that this successful experiment would go forward as a theoretical approach in assisting the building of healthy future generations of children who may have a family history of diseases. Dr Shoukhrat Mitalipov, one of the researchers, claims, “We believe that with the proper governmental approvals, our work can rapidly be translated into clinical trials for humans and eventually approved therapies.” (Paddock 2009).
Ivy Tseng 42034153
For article by Catherine Paddock, PhD 28 August 2009:
http://www.medicalnewstoday.com/articles/162266.php
For original research paper, “Mitochondrial gene replacement in primate offspring and embryonic stem cells” by Masahito Tachibana, Michelle Sparman, Hathaitip Sritanaudomchai, Hong Ma, Lisa Clepper, Joy Woodward, Ying Li, Cathy Ramsey, Olena Kolotushkina and Shoukhrat Mitalipov 26 August 2009:
http://www.nature.com.ezproxy.library.uq.edu.au/nature/journal/vaop/ncurrent/full/nature08368.html
For supplementary information:
http://www.nature.com.eqproxy.library.uq.edu.au/nature/journal/vaop/ncurrent/suppinfo/nature08368.html
