Search

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.

We have used DNA transfection to identify several regions of the adenovirus genome needed to induce replication of the defective parvovirus, adenovirus-associated virus (AAV). Previous studies have indicated that only early adenovirus functions are needed to aid the replication of AAV. In this report, we demonstrate that three restriction endonuclease fragments of adenovirus DNA are necessary for production of infectious AAV in 293-31 cells (an adenovirus type 5-transformed human embryonic kidney cell line). These fragments map from 28.5 to 29.4, 59.5 to 75.9, and 89.7 to 100 map units on the adenovirus type 2 genome and correspond to the locations of the VAI RNA gene, early region 2, and early region 4, respectively. The 293-31 cell line, which has been found to express early region 1A and 1B proteins, alone is incapable of supporting AAV replication or even AAV DNA synthesis. Additional experiments with adenovirus type 5 host range mutants (group I, hr1 and group II, hr7) indicate, however, that early region 1A provides an essential function(s) for AAV replication, whereas early region 1B probably does not.