Publications by authors named "Dieter Ammermann"

It was investigated whether (1) the number of cilia of the dorsal kineties 3 and 4 and (2) the cell length are species-specific characters which can be used to distinguish the sibling species S. mytilus and S. lemnae.

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Ciliated protists are model organisms for a number of molecular phenomena including telomerase function, self-splicing introns, and an RNA interference-related mechanism in programmed DNA elimination. Despite this relevance, our knowledge about promoters and transcriptional regulation in these organisms is very limited. The macronuclear genome of stichotrichous ciliates consists of minichromosomes which typically encode a single gene.

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A differentiation, based on morphological characters, between Stylonychia mytilus and Stylonychia lemnae is very difficult, especially for non-specialists. These two sibling species were considered as one species, S. mytilus, until detailed cytological and genetic studies could show the existence of two genetically isolated varieties.

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Stylonychia lemnae (Ciliophora, Spirotrichea), a member of the Stylonychia mytilus complex, shows a global distribution, occurring in many temperate fresh waters. As there are few descriptions of biogeographical patterns of ubiquitously occurring ciliated protozoans, we report a distinct sequence difference within the small subunit ribosomal DNA gene, which occurs only in the clones of S. lemnae isolated from the surroundings of Ithaca (USA) in comparison with clones of the same species from different regions in Europe, Asia, and South Africa.

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A sexually reproducing hypotrichous ciliates undergo senescence which is in general attributed to degenerative processes in the macronucleus, assuming that loss of viability is based on loss of genetic elements. It is generally accepted that the genetic elements in the macronucleus of hypotrichs segregate randomly, a process which potentially can lead to aneuploid imbalances in the distribution of gene copies. It is, however, unclear whether there are mechanisms which compensate for such imbalances such that each genetic element regains its predetermined copy number (regulatory model, conserving euploidy), or whether the genetic elements only double, so that genetic imbalances can be inherited to further generations (stochastic model, allowing aneuploidy).

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