Linear mitochondrial genomes: 30 years down the line

Nosek, Jozef; Tomáška, Ľubomír; Fukuhara, Hiroshi; Suyama, Yoshitaka; Kováč, Ladislav

doi:10.1016/s0168-9525(98)01443-7

Cited by 117 publications

(83 citation statements)

References 38 publications

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“…Their extremities appear to lack sophisticated decorations, such as covalently closed single-stranded termini or covalently attached proteins. Such structures, which are found in several other linear mitochondrial genomes (26), are notorious for significantly reducing the cloning efficiency of terminal regions (27), a difficulty that was not encountered in the case of A. parasiticum mtDNA.…”

Section: Resultsmentioning

confidence: 99%

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Unique mitochondrial genome architecture in unicellular relatives of animals

Burger

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Zhu

et al. 2003

Proc. Natl. Acad. Sci. U.S.A.

208

118

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Animal mtDNAs are typically small (Ϸ16 kbp), circular-mapping molecules that encode 37 or fewer tightly packed genes. Here we investigate whether similarly compact mitochondrial genomes are also present in the closest unicellular relatives of animals, i.e., choanoflagellate and ichthyosporean protists. We find that the gene content and architecture of the mitochondrial genomes of the choanoflagellate Monosiga brevicollis, the ichthyosporean Amoebidium parasiticum, and Metazoa are radically different from one another. The circular-mapping choanoflagellate mtDNA with its long intergenic regions is four times as large and contains two times as many protein genes as do animal mtDNAs, whereas the ichthyosporean mitochondrial genome totals >200 kbp and consists of several hundred linear chromosomes that share elaborate terminal-specific sequence patterns. The highly peculiar organization of the ichthyosporean mtDNA raises questions about the mechanism of mitochondrial genome replication and chromosome segregation during cell division in this organism. Considering that the closest unicellular relatives of animals possess large, spacious, gene-rich mtDNAs, we posit that the distinct compaction characteristic of metazoan mitochondrial genomes occurred simultaneously with the emergence of a multicellular body plan in the animal lineage. multichromosome mitochondrial genome ͉ linear mtDNA ͉ ancestors of animals ͉ protists

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Section: Resultsmentioning

confidence: 99%

“…Although a dozen or so mitochondrial genomes are known to exist as linear chromosomes, these consist of only a single type of DNA molecule (25)(26)(27). Exceptions are found in four cnidarian classes, including Hydra, whose mtDNA is in two linear pieces (28,29).…”

Section: Resultsmentioning

confidence: 99%

Unique mitochondrial genome architecture in unicellular relatives of animals

Burger

Forget

Zhu

et al. 2003

Proc. Natl. Acad. Sci. U.S.A.

208

118

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“…In minute colonies segregated by another deletion mutant, it was shown that the 1.7-kb deletion encompassing the cob gene had spread into the adjacent gene (Randolph-Anderson et al, 1993), which favors the hypothesis that linear mitochondrial DNA molecules deprived of their left telomeric ends are subject to exonuclease degradation. In this respect, the particular structure of mitochondrial telomeres (Nosek et al, 1998) or the presence of proteins at the termini of some linear plant mitochondrial plasmids (Kemble and Thompson, 1982) could conceivably serve a protective function. The data presented in Tables 3 and 4 indicate that the absence of nd4 and the 3Ј end of nd5 in all dum24 mitochondrial DNA copies is correlated with the loss of complex I activity.…”

Section: Discussionmentioning

confidence: 99%

Alteration of Dark Respiration and Reduction of Phototrophic Growth in a Mitochondrial DNA Deletion Mutant of Chlamydomonas Lacking cob, nd4, and the 3′ End of nd5

Duby

Matagne

1999

Plant Cell

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We describe here a new type of mitochondrial mutation ( dum24 ; for dark uniparental minus inheritance) of the unicellular photosynthetic alga Chlamydomonas reinhardtii . The mutant fails to grow under heterotrophic conditions and displays reduced growth under both photoautotrophic and mixotrophic conditions. In reciprocal crosses between mutant and wild-type cells, the meiotic progeny only inherit the phenotype of the mating-type minus parent, indicating that the dum24 mutation exclusively affects the mitochondrial genome. Digestion with various restriction enzymes followed by DNA gel blot hybridizations with specific probes demonstrated that dum24 cells contain four types of altered mitochondrial genomes: deleted monomers lacking cob , nd4 , and the 3 Ј end of the nd5 gene; deleted monomers deprived of cob , nd4 , nd5 , and the 5 Ј end of the cox1 coding sequence; and two types of dimers produced by end-to-end fusions between monomers similarly or differently deleted. Due to these mitochondrial DNA alterations, complex I activity, the cytochrome pathway of respiration, and presumably, the three phosphorylation sites associated with these enzyme activities are lacking in the mutant. The low respiratory rate of the dum24 cells results from the activities of rotenoneresistant NADH dehydrogenase, complex II, and alternative oxidase, with none of these enzymes being coupled to ATP production. To our knowledge, this type of mitochondrial mutation has never been described for photosynthetic organisms or more generally for obligate aerobes.

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“…Recombination is the primary mechanism of telomere maintenance in the mosquito malarial vector, Anopheles gambiae (Roth et al, 1997), and possibly for the telomeres of linear mitochondrial DNA in some species of yeast (Nosek et al, 1998). Recombination is also used by some species of yeast as a back-up mechanism for telomere maintenance.…”

Section: Telomeric Recombination In Alt+ Cellsmentioning

confidence: 99%

Alternative lengthening of telomeres in mammalian cells

et al. 2002

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Some immortalized mammalian cell lines and tumors maintain or increase the overall length of their telomeres in the absence of telomerase activity by one or more mechanisms referred to as alternative lengthening of telomeres (ALT). Characteristics of human ALT cells include great heterogeneity of telomere size (ranging from undetectable to abnormally long) within individual cells, and ALT-associated PML bodies (APBs) that contain extrachromosomal telomeric DNA, telomere-speci®c binding proteins, and proteins involved in DNA recombination and replication. Activation of ALT during immortalization involves recessive mutations in genes that are as yet unidenti®ed. Repressors of ALT activity are present in normal cells and some telomerase-positive cells. Telomere length dynamics in ALT cells suggest a recombinational mechanism. Inter-telomeric copying occurs, consistent with a mechanism in which singlestranded DNA at one telomere terminus invades another telomere and uses it as a copy template resulting in net increase in telomeric sequence. It is possible that t-loops, linear and/or circular extrachromosomal telomeric DNA, and the proteins found in APBs, may be involved in the mechanism. ALT and telomerase activity can co-exist within cultured cells, and within tumors. The existence of ALT adds some complexity to proposed uses of telomererelated parameters in cancer diagnosis and prognosis, and poses challenges for the design of anticancer therapeutics designed to inhibit telomere maintenance.

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Linear mitochondrial genomes: 30 years down the line

Cited by 117 publications

References 38 publications

Unique mitochondrial genome architecture in unicellular relatives of animals

Unique mitochondrial genome architecture in unicellular relatives of animals

Alteration of Dark Respiration and Reduction of Phototrophic Growth in a Mitochondrial DNA Deletion Mutant of Chlamydomonas Lacking cob, nd4, and the 3′ End of nd5

Alternative lengthening of telomeres in mammalian cells

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