NDLI: Mitochondrial modulation of maternally transmitted antigen: analysis of cell hybrids.

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Mitochondrial modulation of maternally transmitted antigen: analysis of cell hybrids.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Rich, R. R. Hull, R. Huston, M. M. Smith, R. Huston, D. P.
Abstract	Maternally transmitted antigen (Mta) is a murine cell surface class I-like antigen that is defined by specific cytotoxic lymphocyte reactivity. Mta is unique in that its expression requires cooperation between genetic elements both in the Qa/Tla region of chromosome 17 and in the cytoplasm. In view of the known cytoplasmic, and thus maternal, inheritance of mitochondria, we have directly assessed their potential involvement in Mta expression. The mitochondria-specific lethal dye rhodamine 6G (R6G) was used to control the input of mitochondria into cell hybrids. The parental lines, one of BALB/c and one of NZB origin, were known to differ in Mta and mtDNA phenotype. Our data show that most control BALB/c-NZB hybrids expressed the BALB/c Mta phenotype and likewise contained only BALB/c-type mtDNA. The NZB Mta phenotype was not coexpressed in the control hybrids. However, when the mitochondrial contribution from BALB/c was prevented by R6G treatment, the majority of the resultant hybrids expressed only the NZB Mta type and likewise contained only NZB mtDNA. The exceptional R6G-treated hybrids that continued to express the BALB/c Mta phenotype likewise contained only BALB/c mtDNA. Thus, in every case the mtDNA phenotype correlated with the Mta phenotype of the cells. Together, the data support the remarkable conclusion that mitochondria modulate the phenotypic expression of a cell surface molecule.
ISSN	00278424
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	10
Volume Number	82
Language	English
Publisher	National Academy of Sciences
Publisher Date	1985-06-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	DNA, Mitochondrial Genetics Histocompatibility Antigens Major Histocompatibility Complex Mice, Inbred Strains Animals Antigens, Surface DNA Restriction Enzymes Gene Expression Regulation Hybrid Cells Physiology Mice Mitochondria Drug Effects Phenotype Rhodamines Pharmacology Research Support, U.S. Gov't, P.H.S. Multidisciplinary
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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