Document Detail


The fate of human sperm-derived mtDNA in somatic cells.
MedLine Citation:
PMID:  9382109     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Inheritance of animal mtDNA is almost exclusively maternal, most likely because sperm-derived mitochondria are actively eliminated from the ovum, either at or soon after fertilization. How such elimination occurs is currently unknown. We asked whether similar behavior could be detected in somatic cells, by following the fate of mitochondria and mtDNAs after entry of human sperm into transformed cells containing mitochondria but lacking endogenous mtDNAs (rho0 cells). We found that a high proportion (10%-20%) of cells contained functioning sperm mitochondria soon after sperm entry. However, under selective conditions permitting only the survival of cells harboring functional mtDNAs, only approximately 1/10(5) cells containing sperm mitochondria survived and proliferated. These data imply that mitochondria in sperm can enter somatic cells relatively easily, but they also suggest that mechanisms exist to eliminate sperm-derived mtDNA from somatic cells, mechanisms perhaps similar to those presumed to operate in the fertilized oocyte.
Authors:
G Manfredi; D Thyagarajan; L C Papadopoulou; F Pallotti; E A Schon
Related Documents :
12799419 - Intracellular clusterin causes juxtanuclear aggregate formation and mitochondrial alter...
20837069 - What makes the mitochondria a killer? can we condition them to be less destructive?
17011159 - Berberine induces apoptosis through a mitochondrial/caspase pathway in human promonocyt...
19805739 - Cell-cell and intracellular lactate shuttles.
4462569 - Differences in the products of mitochondrial protein synthesis in vivo in human and mou...
15589839 - Influence of a mitochondrial genetic defect on capacitative calcium entry and mitochond...
2748939 - Cell proliferation and differentiation in squamous cancer.
24221569 - Preprophase bands of microtubules and the cell cycle: kinetics and experimental uncoupl...
21427009 - Angiopep-conjugated poly(ethylene glycol)-co-poly(ε-caprolactone) nanoparticles as dua...
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  American journal of human genetics     Volume:  61     ISSN:  0002-9297     ISO Abbreviation:  Am. J. Hum. Genet.     Publication Date:  1997 Oct 
Date Detail:
Created Date:  1997-11-07     Completed Date:  1997-11-07     Revised Date:  2009-11-18    
Medline Journal Info:
Nlm Unique ID:  0370475     Medline TA:  Am J Hum Genet     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  953-60     Citation Subset:  IM    
Affiliation:
H. Houston Merritt Clinical Research Center for Muscular Dystrophy and Related Disorders, and Department of Neurology, Columbia University College of Physicians and Surgeons, New York, NY 10032, USA.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Animals
Cell Survival
Clone Cells
DNA, Mitochondrial / analysis*,  genetics
Electron Transport Complex IV / analysis,  biosynthesis
Female
Genetic Markers
Humans
Male
Mitochondria / metabolism*,  ultrastructure
Polymerase Chain Reaction / methods
Polymorphism, Restriction Fragment Length
Sperm-Ovum Interactions*
Spermatozoa / physiology*
Transfection
Grant Support
ID/Acronym/Agency:
AG12131/AG/NIA NIH HHS; HD32062/HD/NICHD NIH HHS; NS28828/NS/NINDS NIH HHS
Chemical
Reg. No./Substance:
0/DNA, Mitochondrial; 0/Genetic Markers; EC 1.9.3.1/Electron Transport Complex IV
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  Risk reversals in predictive testing for Huntington disease.
Next Document:  Deletion of all CGG repeats plus flanking sequences in FMR1 does not abolish gene expression.