Better Mitochondrial Replacement: But Why? 
        
            By Ricki Lewis, 
                PLOS
             | 06. 09. 2016
        
                    
                                    
                    
                                                                                                                                    
                                                                            
                              
    
  
  
    
  
          
  
      
    
            The disconnect was striking between the headline of the news release a few days ago – “Improved method for mitochondrial replacement therapy” – and the title of the paper to which it refers – “Towards clinical application of pronuclear transfer to prevent mitochondrial DNA disease.”
 
  The news release reported changes in the experimental protocol for   pronuclear transfer (PNT) a proposed way to prevent mitochondrial   disease. Pronuclei house the genomes in egg and sperm. PNT places them   into human fertilized ova whose nuclei have been removed, but whose   mitochondria remain in the cytoplasm. The intent is to fashion   fertilized ova missing the mitochondria from a woman who has a   mitochondrial mutation, which she’d know from having a child with one of   the dozen or so diseases caused by mutations in mitochondrial genes. (Additional conditions that affect mitochondria result from mutations in genes in the nucleus).
 
  The paper, published yesterday online in Nature,   is from Mary Herbert and colleagues at the Wellcome Trust Centre for   Mitochondrial Research, Newcastle upon Tyne, United Kingdom.
 
   It’s a clear, concise report of technically elegant and...
 
       
 
  
 
    
    
  
   
                        
                                                                                
                 
                                                    
                            
                                  
    
  
  
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