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Mitochondrial Replacement, Evolution, and the Clinic

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Mitochondrial Replacement, Evolution, and the Clinic POLICYFORUM MEDICINE Mitochondrial replacement therapy might bear Mitochondrial Replacement, health risks, especially for males. Evolution, and the Clinic Klaus Reinhardt, 1, 2* Damian K. Dowling, 3 Edward H. Morrow 4 itochondrial diseases [often caused the United Kingdom, who suggested that available to couples at risk of having an by mutations in mitochondrial MR will not affect characteristics normally affected child” (9). The results, published MDNA (mtDNA)] can manifest associated with individual identity (6). MR in March 2013, note general support within in a range of severe symptoms, for which was compared with replacing the batteries the United Kingdom for permitting MR; if there are currently no cures (1). The applied under strict regulation, such diseases are passed from mothers to Health outcomes of intraspecies as case-by-case approval of licensed offspring. Intense research efforts experimental mr in animals hospitals, ethical concerns about the have recently focused on a germline implementation of MR were consid- Studies using invasive techniques therapeutic strategy to prevent the ered to be outweighed by arguments inheritance of disease-causing mito- Human (Homo sapiens) in favor of MR (10). In June 2013, chondria. However, although there has Development to blastocyst stage the British government announced Normal gene expression and metabolic profile in cell lines been increased government interest, they will produce draft regulations especially in the United Kingdom, for Macaque (Macaca mulatta) on therapeutic MR for further public Normal embryo development and metabolic profile at juvenile age using this approach to treat patients, consultation, to be debated in parlia- there are reasons to believe that it is Mouse (Mus musculus) ment in 2014 (11). Altered respiration and growth in mouse hybrid cell line premature to move this technology Much of the scientific debate into the clinic at this stage. has focused on genetic factors that on September 24, 2013 Studies using genetic crossing techniques Early experiments in mice pro- are well known to affect mitochon- duced disease-free oocytes by means Mouse (Mus musculus) drial disease, which typically devel- of mitochondrial replacement (MR): Normal survival to adulthood ops only if the relative amount of Reduced growth, exercise ability, learning in adult the fertilized nucleus from an oocyte mutated, relative to healthy, mtDNA laden with mitochondria carry- Fruit fly (Drosophila melanogaster) in any given tissue surpasses a criti- Altered juvenile viability ing mtDNA mutations was injected Altered nuclear gene expression in adult cal threshold (1, 10). These frequen- into the cytoplasm of an enucleated Altered, aging mostly in adult cies can shift rapidly at embryogen- donor oocyte that carried mutation- Altered, often reduced, fertility in adult esis. If any mutant mtDNA remains www.sciencemag.org free mitochondria (2). A break- Seed beetle (Callosobruchus maculatus) in an enucleated oocyte after MR, the through in primates came when four Altered development time and metabolic rate children might be at risk of develop- macaque babies were born after Altered fertility in adult ing the disease or passing the patho- MR-assisted in vitro fertilization Altered survival in adult genic mutation on to their offspring. (IVF) (3) and when human embryos Copepod (Tigriopus californicus) As a result, the HFEA considered survived intact after MR to the blas- Reduced juvenile viability whether only male embryos should tocyst stage (4). Consequently, the Reduced mitochondrial function and ATP production in adults be allowed to develop post-MR, to British government commissioned ensure that no mutations are inadver- Downloaded from the Human Fertilisation and Embry- Health outcomes of intraspecies experimental MR in animals. tently transmitted after the treatment. ology Authority (HFEA) to col- Studies either invasively removed the nucleus by placing it into the This body of research was carefully lect evidence as to the suitability of enucleated donor oocyte (blue shading) or replaced mitochondria by considered by the HFEA, and we do MR as a therapeutic approach. The repeatedly crossing foreign mitochondrial genotypes into nuclear back- not review it here (10). HFEA urged further experiments grounds (green shading) (see table S1 for details). All species share the Rather, we draw attention to the- same 37 mitochondrial encoded genes. Studies of health effects of MR on before clinical use of MR (5). The ory and experimental findings that vertebrates that have reached reproductive ages are lacking. U.K. Nuffield Council on Bioeth- appear to have been overlooked in the ics initiated an ethical review of MR and of a camera (6), an analogy picked up by the scientifi c and public forums of this debate. concluded it was ethically acceptable (6). popular press. Studies on model organisms, ranging from This view was supported by the Medical Subsequently, the four macaques born mice to fruit fl ies, indicate that MR can pro- Research Council and Wellcome Trust of after MR were shown to be healthy at 3 years foundly change the expression profiles of of age (7), and technical difficulties have nuclear genes and affect a range of impor- 1Animal Evolutionary Ecology, University of Tuebingen, been reduced in human blastocysts (7, 8). tant traits such as individual development, 72076 Tuebingen, Germany. 2Department of Animal and These results were used to urge the U.S. Food cognitive behavior, and key health parame- Plant Sciences, University of Sheffi eld, Sheffi eld S10 2TN, UK. 3School of Biological Sciences, Monash University, 3800 and Drug Administration to review its fund- ters. These studies also suggest that males of Victoria, Australia. 4Evolution, Behaviour, and Environment ing policy on gene therapy (7). reproductive age are particularly sensitive to Group, School of Life Sciences, University of Sussex Brighton The HFEA then was asked to initiate MR-induced effects. BN1 9QG, UK. a public consultation into the question of Natural genetic differences in the mtDNA *Corresponding author. [email protected] whether MR-assisted IVF “should be made sequence exist from one individual to another, www.sciencemag.org SCIENCE VOL 341 20 SEPTEMBER 2013 1345 Published by AAAS POLICYFORUM broadly denoted as mtDNA haplotypes. Puta- effects were naturally occurring, putatively In conclusion, recent technical advances tively healthy mitochondrial haplotypes dif- healthy variants. Hundreds of mitochondrial- suggest that MR-assisted gene therapy could fer in their effect on the expression of key sensitive nuclear genes identifi ed in that study soon be available to help female sufferers of health and performance parameters. In par- had a core role in male fertility. For example, mitochondrial diseases have healthy chil- ticular, energy production critically hinges on one of the fi ve combinations in which mito- dren, and this is clearly an exciting pros- extensive cross-talk between genes dispersed chondrial-nucleus interactions were disrupted pect. Changing legislation that would facili- across the nucleus and the mitochondria (12). by mismatching was completely male-ster- tate this technique will require a debate over Because phenotypes with less-than-ideal ile but female-fertile (14). In other fl y stud- the extent to which the results and principles cross-talk are disfavored by natural selection, ies, MR resulted in male-biased modifica- outlined here are ethically and clinically rele- coordinated mitochondrial-nuclear interac- tions to components of aging and affected vant to MR in humans. MtDNA diseases vary tions become highly specifi c over evolution- the outcomes of in vivo male fertility (see from mild symptoms and learning disabilities ary time. If MR disrupts such specifi c, highly the table). Together, these results suggest that to severe disabilities and premature death. coordinated mito-nuclear allelic interactions, core components of male health depend on Assessing the costs and benefi ts of MR treat- adverse health outcomes might occur. fi ne-tuned coordination between mitochon- ment requires that prospective patients are This prediction is supported by experi- drial and nuclear gene complexes, and thus as fully informed as possible. The difference mental studies reporting the expression of the HFEA conclusion that “there is no evi- across patients in the severity of expected off- disease phenotypes when genetic backcross- dence for any mismatch between the nucleus spring symptoms in the event that MR treat- ing was used to replace mitochondria and and any mtDNA haplogroup, at least within ment is not taken will shape the decision of to create intergenomic mismatches in mice. a species” [(10), 6.17 on p. 17] is incomplete choosing the treatment versus waiting for the Altered respiratory metabolism and reduced and unsubstantiated. outcomes of further research. Some families performance, learning, and exploratory Two points may deserve careful consid- who are predicted to be, or who have previ- capacity in males were reported when mito- eration prior to any change in legislation. ously conceived offspring that were, severely chondrial-nuclear genomic interactions were First, studies in humans have only tracked affl icted by mtDNA diseases are more likely experimentally mismatched (see the table and health through to the blastocyst stage and in to be prepared to take the risk. Others whose table S1). Females were not tested in those macaques to 3 years of age (see the table). The
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