Non-mendelian inheritance of the HET-s prion or HET-s prion domains determines the het-S spore killing system in Podospora anserina

Dalstra, H.J.P.; Zee, Remko van der; Swart, K.; Hoekstra, Rolf F.; Saupe, Sven J.; Debets, A.J.M.

doi:10.1016/j.fgb.2005.05.004

Cited by 27 publications

(22 citation statements)

References 27 publications

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“…The studies of SD, het-s, Sk, and other examples described by Lyttle (1991a,b), Dalstra et al (2003Dalstra et al ( , 2005, and Burt and Trivers (2006) show that there are several diverse cellular mechanisms that can trigger meiotic drive. However, the Podospora [Het-s] prion, the Drosophila SD locus, and the mouse t locus are the only three meiotic drive elements that have been characterized at the molecular level (Schimenti 2000;Kusano et al 2001Kusano et al , 2003Maddelein et al 2002;Dalstra et al 2003Dalstra et al , 2005.…”

Section: Discussionmentioning

confidence: 94%

“…However, the Podospora [Het-s] prion, the Drosophila SD locus, and the mouse t locus are the only three meiotic drive elements that have been characterized at the molecular level (Schimenti 2000;Kusano et al 2001Kusano et al , 2003Maddelein et al 2002;Dalstra et al 2003Dalstra et al , 2005. For example, SD in Drosophila causes preferential transmission of SD chromosomes because SD 1 -bearing spermatids fail to mature in SD/SD 1 males.…”

Section: Discussionmentioning

confidence: 99%

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Neurospora Spore KillersSk-2andSk-3Suppress Meiotic Silencing by Unpaired DNA

2007

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In Neurospora crassa, pairing of homologous DNA segments is monitored during meiotic prophase I. Any genes not paired with a homolog, as well as any paired homologs of that gene, are silenced during the sexual phase by a mechanism known as meiotic silencing by unpaired DNA (MSUD). Two genes required for MSUD have been described previously: sad-1 (suppressor of ascus dominance), encoding an RNAdirected RNA polymerase, and sad-2, encoding a protein that controls the perinuclear localization of SAD-1. Inactivation of either sad-1 or sad-2 suppresses MSUD. We have now shown that MSUD is also suppressed by either of two Spore killer strains, Sk-2 and Sk-3. These were both known to contain a haplotype segment that behaves as a meiotic drive element in heterozygous crosses of killer 3 sensitive. Progeny ascospores not carrying the killer element fail to mature and are inviable. Crosses homozygous for either of the killer haplotypes suppress MSUD even though ascospores are not killed. The killer activity maps to the same 30-unit-long region within which recombination is suppressed in killer 3 sensitive crosses. We suggest that the region contains a suppressor of MSUD. S EXUAL reproduction in Neurospora crassa is mediated by the fusion of two haploid nuclei that carry compatible mating-type genes (mat A and mat a). The haploid nuclei proliferate in specialized premeiotic ascogenous tissue (precroziers and three-celled croziers) within the fertilized fruiting body (perithecium). Two nuclei of opposite mating type that are sequestered in the subapical cell of the crozier then migrate into a tubular sac (ascus) and fuse to create the zygote, which immediately undergoes two meiotic divisions and a postmeiotic mitosis. The resulting eight haploid nuclei reside in the same cytoplasm until they are sequestered into eight linearly ordered ascospores. The mating-type locus and other segregating markers show 1:1 segregation (Raju 1992;Davis 2000).Meiotic drive is a phenomenon in which certain chromosomal loci show a progeny ratio different from 1:1 and one allele is favored over the other. Examples of meiotic drive in animals include the segregation distorter (SD) system of Drosophila melanogaster and the t haplotype in the mouse (Lyttle 1991a,b;Schimenti 2000;Kusano et al. 2003). In heterozygous males, the meiotic products that do not carry the drive element (SD chromosome or t haplotype) fail to differentiate into functional sperm. Although meiotic drive is widespread in insects, mammals, plants, and fungi, very few cases have been dissected at the molecular level (Pennisi 2003;Burt and Trivers 2006).In Neurospora, Spore killers are chromosomal elements that cause the death of ascospores that do not contain the killer element (Turner and Perkins 1979, 1991). For example, in a cross of Spore killer 3 wild type (Sk sensitive), every mature ascus contains four normalsized, black, viable ascospores and four tiny, undeveloped ascospores that are inviable (see Figure 2A). All survivors carry the killer element. When both kill...

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Section: Discussionmentioning

confidence: 94%

Section: Discussionmentioning

confidence: 99%

Neurospora Spore KillersSk-2andSk-3Suppress Meiotic Silencing by Unpaired DNA

2007

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“…15) and selective spore killing in Podospora anserina. 16 These functions are clearly distinct from the roles assigned to cellular PrP in the central nervous system (see refs. 17 and 18 and references therein).…”

confidence: 98%

Prion-Prion Interactions

Derkatch

Liebman²

2007

Prion

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Published previously online as a Prion AbStrActThe term prion has been used to describe self-replicating protein conformations that can convert other protein molecules of the same primary structure into its prion conformation. Several different proteins have now been found to exist as prions in Saccharomyces cerevisiae. Surprisingly, these heterologous prion proteins have a strong influence on each others' appearance and propagation, which may result from structural similarity between the prions. Both positive and negative effects of a prion on the de novo appearance of a heterologous prion have been observed in genetic studies. Other examples of reported interactions include mutual or unilateral inhibition and destabilization when two prions are present together in a single cell. In vitro work showing that one purified prion stimulates the conversion of a purified heterologous protein into a prion form, suggests that facilitation of de novo prion formation by heterologous prions in vivo is a result of a direct interaction between the prion proteins (a cross-seeding mechanism) and does not require other cellular components. However, other cellular structures, e.g., the cytoskeleton, may provide a scaffold for these interactions in vivo and chaperones can further facilitate or inhibit this process. Some negative prion-prion interactions may also occur via a direct interaction between the prion proteins. Another explanation is a competition between the prions for cellular factors involved in prion propagation or differential effects of chaperones stimulated by one prion on the heterologous prions.

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“…If the het-s expression stops during the sexual cycle, the late asci would inherit fewer prion seeds and thus killing percentages would diminish. 27 An alternative hypothesis, is that the progressive build up of the HET-S protein in the ascogonium during perithecial maturation leads to curing of the [Het-s] prion in late asci. Indeed, it is important to note that in this cross, the majority of the het-s ascospores are cured from the prion (even though the maternal parent was [Het-s]), this loss of [Het-s] indicates that het-S exerts a prion curing effect in a large fraction of the asci.…”

Section: An Infectious Protein Encoded By An Invasive Allelementioning

confidence: 99%