caa a22 4500 469044705 CHVBK 20180323132821.0 cr unu---uuuuu 170328e19920701xx s 000 0 eng 10.1007/BF01799602 doi (NATIONALLICENCE)springer-10.1007/BF01799602 Clayton D. Department of Developmental Biology, Stanford University School of Medicine, 94305-5427, Stanford, CA, USA aut Structure and function of the mitochondrial genome [Elektronische Daten] [D. Clayton] Summary: It is now clear that molecular defects in human mitochondrial DNA play a significant role in human disease. Mitochondrial DNA mutations range from single base changes in the 16.5 kilobase-pair genome up to large deletions and rearrangements. Independently of the actual cause of a given mutation, it is possible to predict at least some of the consequences of changes in mitochondrial DNA sequence. This paper reviews our overall understanding of the mode and mechanism of mitochondrial DNA replication and transcription and how this relates to mitochondrial gene expression. This provides a background to anticipate the nature and extent of mitochondrial DNA sequence changes that might be of physiological consequence. SSIEM and Kluwer Academic Publishers, 1992 Journal of Inherited Metabolic Disease Kluwer Academic Publishers 15/4(1992-07-01), 439-447 0141-8955 15:4<439 1992 15 10545 https://doi.org/10.1007/BF01799602 text/html Onlinezugriff via DOI 1 research-article jats NATIONALLICENCE 856 40 https://doi.org/10.1007/BF01799602 text/html Onlinezugriff via DOI NATIONALLICENCE 100 1- Clayton D. Department of Developmental Biology, Stanford University School of Medicine, 94305-5427, Stanford, CA, USA aut NATIONALLICENCE 773 0- Journal of Inherited Metabolic Disease Kluwer Academic Publishers 15/4(1992-07-01), 439-447 0141-8955 15:4<439 1992 15 10545 Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer