The putative origin of heavy strand replication (oriH) in mitochondrial DNA is highly conserved among the teleost fishes

DNA Sequence ◽  
1993 ◽  
Vol 3 (6) ◽  
pp. 397-399 ◽  
Author(s):  
Steinar Johansen ◽  
Terje Johansen
1986 ◽  
Vol 6 (9) ◽  
pp. 3262-3267
Author(s):  
D D Chang ◽  
D A Clayton

Transcription of the heavy strand of mouse mitochondrial DNA starts from two closely spaced, distinct sites located in the displacement loop region of the genome. We report here an analysis of regulatory sequences required for faithful transcription from these two sites. Data obtained from in vitro assays demonstrated that a 51-base-pair region, encompassing nucleotides -40 to +11 of the downstream start site, contains sufficient information for accurate transcription from both start sites. Deletion of the 3' flanking sequences, including one or both start sites to -17, resulted in the initiation of transcription by the mitochondrial RNA polymerase from alternative sites within vector DNA sequences. This feature places the mouse heavy-strand promoter uniquely among other known mitochondrial promoters, all of which absolutely require cognate start sites for transcription. Comparison of the heavy-strand promoter with those of other vertebrate mitochondrial DNAs revealed a remarkably high rate of sequence divergence among species.


2021 ◽  
Author(s):  
Hiroshi Sugiyama ◽  
Vinodh Sahayasheela ◽  
Zutao Yu ◽  
Ganesh Pandian

Abstract G-quadruplexes (G4s) are noncanonical structures that can form in the genomes of a range of organisms and are known to play various roles in cellular function. G4s can also form in mitochondrial DNA (mtDNA) because of their high guanine content, and these G4s may play roles in regulating gene expression, DNA replication, and genome stability. However, little is known regarding the evolution and dissemination of G4s in mitochondria. Here we analyzed the potential G4-forming sequences in mtDNA of 16 species from various families and demonstrated that the heavy strand of mtDNA of higher-order organisms contained higher levels of G4 regions than that of lower-order organisms. Analysis of the codons in the light strand revealed enrichment of guanine/cytosine-rich regions in higher eukaryotes and of adenine/thymidine-rich regions in lower-order organisms. Our study showed the diversity of G4s in species ranging from lower to higher orders. In particular, mammals such as humans, chimpanzees, and monkeys display a greater number of G4s than lower-order organisms. These potentially play a role in a range of cellular functions and assist in the evolution of higher organisms.


Genetics ◽  
1991 ◽  
Vol 128 (2) ◽  
pp. 393-403 ◽  
Author(s):  
J M Cornuet ◽  
L Garnery ◽  
M Solignac

Abstract The mitochondrial genome of honeybees is characterized by the presence of a long intergenic sequence located between the COI and COII genes. In addition, the length of this sequence varies between and within subspecies. Four length categories (200, 250, 450 and 650 bp) have been found in 63 sampled colonies. Analysis of the sequence of the largest type reveals the existence of two units: P (54 bp, 100% A + T) and Q (196 bp, 93.4% A + T). The lengths encountered in the sample are explained by the following combinations: Q, PQ, PQQ and PQQQ. According to similarities in primary and secondary structures, the sequence Q has been divided into three parts: Q1 (similar to the 3' end of the COI gene), Q2 (similar to the neighboring tRNA(leu) gene) and Q3 (highly similar to the P sequence). These relationships led us to hypothesize that these sequences, which do not have any counterpart in Drosophila yakuba mitochondrial DNA (mtDNA), arose by tandem duplication. The usual location of length variation in mtDNA control regions prompted us to examine the hypothesis that this COI-COII intergenic region might contain an origin of replication. High A + T content, stability profile, hairpin and cloverleaf putative secondary structures are all in favor of this hypothesis.


1991 ◽  
Vol 11 (3) ◽  
pp. 1631-1637
Author(s):  
C T Moraes ◽  
F Andreetta ◽  
E Bonilla ◽  
S Shanske ◽  
S DiMauro ◽  
...  

We identified two patients with progressive external ophthalmoplegia, a mitochondrial disease, who harbored a population of partially deleted mitochondrial DNA (mtDNA) with unusual properties. These molecules were deleted from mtDNA positions 548 to 4,442 and encompassed not only rRNA sequences but the heavy-strand promoter region as well. A 13-bp direct repeat was found flanking the breakpoint precisely, with the repeat at positions 535 to 547 located within the binding site for mitochondrial transcription factor 1 (mtTF1). This is the second mtDNA deletion involving a 13-bp direct repeat reported but is at least 10 times less frequent in the patient population than the former one. In situ hybridization studies showed that transcripts under the control of the light-strand promoter were abundant in muscle fibers with abnormal proliferation of mitochondria, while transcripts directed by the heavy-strand promoter, whether of genes residing inside or outside the deleted region, were not. The efficient transcription from the light-strand promoter implies that the major heavy-and light-strand promoters, although physically close, are functionally independent, confirming previous in vitro studies.


1986 ◽  
Vol 6 (9) ◽  
pp. 3262-3267 ◽  
Author(s):  
D D Chang ◽  
D A Clayton

Transcription of the heavy strand of mouse mitochondrial DNA starts from two closely spaced, distinct sites located in the displacement loop region of the genome. We report here an analysis of regulatory sequences required for faithful transcription from these two sites. Data obtained from in vitro assays demonstrated that a 51-base-pair region, encompassing nucleotides -40 to +11 of the downstream start site, contains sufficient information for accurate transcription from both start sites. Deletion of the 3' flanking sequences, including one or both start sites to -17, resulted in the initiation of transcription by the mitochondrial RNA polymerase from alternative sites within vector DNA sequences. This feature places the mouse heavy-strand promoter uniquely among other known mitochondrial promoters, all of which absolutely require cognate start sites for transcription. Comparison of the heavy-strand promoter with those of other vertebrate mitochondrial DNAs revealed a remarkably high rate of sequence divergence among species.


1986 ◽  
Vol 6 (5) ◽  
pp. 1446-1453 ◽  
Author(s):  
D D Chang ◽  
D A Clayton

The major transcriptional control sequences of vertebrate mitochondrial DNA lie within the displacement loop region. Transcription events initiating in the displacement loop sequence of the mouse genome were identified by 5' end mapping of primary transcripts by S1 nuclease protection and primer extension techniques. Light-strand transcription initiates at a single site, 165 nucleotides upstream of the major heavy-strand origin of replication. Transcription of the heavy strand occurs at two distinct sites, 5 and 13 nucleotides upstream of the gene for phenylalanyl-tRNA, the first heavy-strand-encoded gene. This spatial relationship of the two transcriptional start sites with each other and with the origin of heavy-strand replication and the gene for tRNAPhe is quite similar to that for human mitochondrial DNA. The predominant form of primary heavy-strand transcript in mouse is a short, ca. 75-nucleotide, RNA containing the sequences of tRNAPhe and a few additional nucleotides at the 5' end of tRNAPhe, suggesting that the processing of tRNA involves independent cleavages at the 5' and 3' ends of tRNA sequences.


Genetics ◽  
1990 ◽  
Vol 124 (1) ◽  
pp. 157-163 ◽  
Author(s):  
N E Buroker ◽  
J R Brown ◽  
T A Gilbert ◽  
P J O'Hara ◽  
A T Beckenbach ◽  
...  

Abstract Extensive length polymorphism and heteroplasmy (multiple forms within an individual) of the D-loop region are observed in mitochondrial DNA of the white sturgeon (Acipenser transmontanus). The nucleotide sequence of this region, for both a short and a long form, shows that the differences are due to variable numbers of a perfect 82-bp direct repeat. We propose a model for the replicative origin of length differences, involving a competitive equilibrium between the heavy strand and the D-loop strand. This model suggests that frequent misalignment in the repeat region prior to elongation, facilitated by a stable secondary structure in the displaced strand, can explain both the polymorphism and heteroplasmy in this species.


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