National Repository of Grey Literature 21 records found  1 - 10nextend  jump to record: Search took 0.01 seconds. 
triggers of asexual reproduction: on the crosslink between hybridization, asexuality, polyploidy and speciation on example of Cobitidae loaches
Marta, Anatolie ; Janko, Karel (advisor) ; Arai, Katsutoshi (referee) ; Trachtulec, Zdeněk (referee)
(in English) Sexual reproduction is considered a nearly universal feature of all eukaryotic organisms and has been hypothesized to be their ancestral state. Sexual reproduction is mainly represented by meiotic division, recombination, production of haploid gametes and fertilization. Although molecular and cytological mechanisms underlying meiosis are highly conservative they may be disrupted in numerous ways leading to the emergence of so-called asexual lineages. The proximate origins of asexuality may differ for particular taxa. In vertebrates, asexuality frequently is triggered by interspecific hybridization. Nowadays "classical" theories predict that asexuals should not be able to persist on a long-term evolutionary scale. However, the hybrid lineages have to overcome short-term disadvantages, such as postzygotic barriers ranging from complete hybrid sterility to altered meiosis resulting in asexual reproduction and even ploidy elevation. Despite that hybrid sterility is one of the most common outcomes of interspecific hybridization, however various lineages found their ways to alleviate these problems and produce viable clonal gametes. The knowledge about proximate mechanisms of unreduced gamete formation in asexual lineages is very limited as many studies were restricted due to methodological...
The effects of epigenetic factor PRDM9 on the fertility of rodent females
Gašić, Srdan ; Trachtulec, Zdeněk (advisor) ; Děd, Lukáš (referee) ; Fulková, Helena (referee)
The Prdm9 gene encodes a histone-3-lysine-4,36-trimethyltransferase that specifies meiotic recombination sites and guides programmed double-strand breaks (DSBs) in mice, rats, and humans. Some vertebrates lost Prdm9 but not fertility throughout evolution, while the removal of Prdm9 caused sterility in some mouse strains, such as C57BL/6 (B6). The reasons for such species-specific fertility differences are unknown. To resolve these different requirements for PRDM9 in fertility, we produced Prdm9 mutants in another mammalian species, Rattus norvegicus, strain SHR/OlaIpcv. The removal of Prdm9 function did not completely abolish fertility in rats (as in B6 mice). Here I demonstrate that the loss of rat PRDM9 delayed female meiosis and caused synapsis and DSB repair defects that lead to a significant oocyte loss. However, unlike Prdm9-deficient B6 mouse oocytes, about 10-15% of pachytene-like mutant rat oocytes synapsed their chromosomes and repaired DSBs to the levels similar to controls. Because of this, female rats lacking PRDM9 maintained some oocytes until adulthood and yielded offspring, while B6 mice lost oocytes around the time of birth. Nevertheless, the adult rat mutant oocytes were exhausted earlier than the control adult rat oocytes. Therefore, PRDM9-lacking female rats suffered from...
Genes of early meiotic prophase I of spermatogenesis in house mouse
Škaloudová, Eliška ; Trachtulec, Zdeněk (advisor) ; Forman, Martin (referee)
Meiosis is an essential cellular process that is necessary for gamete formation in all sexually reproducing organisms. This work is focused on the description of the genes of early stages of meiotic division in males of a mammalian model, the house mouse. The first part summarizes meiosis focusing on prophase I, which is longer than prophase II. Prophase I is divided into five stages, namely leptotene, zygotene, pachytene, diplotene, and diakinesis. Mouse spermatogenesis and its differences from oogenesis are also briefly described. The second part provides a list of genes encoding proteins required for initiation of meiotic division, pairing and synapses of chromosomes, and initiation of the catalysis of double-strand breaks. Double-strand breaks are repaired by homologous recombination, which may result in so-called crossing-over, the major source of genetic variability. The work deals with the early stage of homologous recombination and components required for this process. Localization of meiotic double-strand breaks in the genome is not random and is under the control of the Prdm9 gene, which seems to take multiple roles, such as the formation of new subspecies of the house mouse. Knowledge of the genes controlling the early stages of meiotic division is a prerequisite to understanding some of...
Genetic interactions of the Prdm9 gene
Šebestová, Lenka ; Trachtulec, Zdeněk (advisor) ; Král, Jiří (referee)
The Prdm9 gene (PR domain containing 9, Meisetz, Hybrid sterility 1) encodes enzyme that trimethylates histone 3 on lysines 4 and 36. These methylation marks determine the positions of DNA double-strand breaks that are repaired by meiotic homologous recombination. In this study, we assayed genetic interactions of Prdm9 with two genes important for spermatogenesis - Mili (Piwil2) involved in piRNA biogenesis and Mybl1 encoding transcription factor that regulates many genes important for prophase I, including piRNA precursors. We crossed laboratory mice carrying mutation in Prdm9 with heterozygotes for mutation in Mybl1 or Mili, and created compound heterozygotes and, in case of Mybl1, also double homozygotes. We assessed body weight and male fertility parameters (weight of testes, sperm count, malformed sperm, percentage of tubules containing spermatocytes and of abnormal nuclei of pachytene spermatocytes) of these mice and compared them to controls. We also investigated the effect of Mybl1 and Mili mutations on fecundity of F1 intersubspecific hybrids. Our results revealed possible interactions of Prdm9 and Mybl1 in the laboratory mouse. Decreased gene dosage of Mybl1 reduced fertility of intersubspecific F1 hybrids. Interaction between Prdm9 and Mili in both laboratory mouse and F1 hybrids remain...
The role of cohesin genes in the meiosis of male house mouse
Šebestová, Lenka ; Trachtulec, Zdeněk (advisor) ; Král, Jiří (referee)
Cohesin genes play an important role in cell division. They ensure proper chromosome segregation during mitosis and meiosis. This study is focused on the role of cohesin genes during meiosis in male house mouse (Mus musculus). At first, this study introduces key processes of mammalian meiosis. Next, the structure of cohesin complex is described; it consists of a heterodimer SMC proteins - SMC3 and SMC1α or SMC1β, which are enclosed to the ring by cleavable subunit RAD21, RAD21L or REC8. Fourth subunit - a STAG protein (STAG1, STAG2 or STAG3) associates with the cleavable subunit. Meiotic function of specific cohesin proteins (SMC1β, RAD21L, REC8 and STAG3) as deduced from the phenotypes of the deficiencies of their genes in male mouse is depicted. All these four genes are necessary for many processes during meiosis, - e.q. sister chromatid cohesion maintenance, synapsis and recombination. STAG3, SMC1β, and REC8 are necessary for centromeric cohesion. STAG3 and RAD21L are important for the assembly of the remaining cohesin subunits. The most important phenotype of deficiency of all four genes is the complete meiotic arrest in male prophase I. Therefore, cohesin research is important for the investigation of the causes of sterility in mammals. key words: cohesin, meiosis, spermatogenesis, mouse,...
Positional cloning of the Hybrid sterility 1 gene: fine genetic mapping and evaluation of two candidate genes
Mihola, Ondřej ; Trachtulec, Zdeněk (advisor) ; Munclinger, Pavel (referee) ; Pravenec, Michal (referee)
Summaryofpublications 1. Positionalcloningof the Hybridsterility1 gene:finegenetic mappingand evaluationof twocandidategenes Hybridsteri|iýis one of the mechanismsof speciation.The Hybridsteriliý1 (HsÍí)genewasthefirstmappedmammaliangene.The geneaffectsfertiliýof male hybridsbetweencertainlaboratorystrains(suchas C57Bl/10)and Mus musculus musculusmiceby causinga breakdownof spermatogenesisat thestageof primary spermatocytes.|ntheprocessof positiona|c|oningoftheHsÍígene,Wegenerateda contigof bacterialartificialchromosomes(BACs)and subsequentlya lowcoverage sequenceof the candidateregionof the '12951/SvlmJstrain.New geneticmarkers narroweddown the HsÍíregionfrom 580 to 360 ki|obases.The productsof two genesfromthisregion,TATA-bindingprotein(Ibp)and proteasomesubunitbeta1 (Psmb1\,accumulateduringspermatogenesis.The proteinshave been described previouslyas having conservedC{erminal sequencesand species-specificN- termini.We eva|uatedthe candidacyof thesegenesfor Hsťíby a||e|icsequencing and by real-timereverse-transcriptionPCR of testicularmRNAs.The resultssuggest thatneitherthePsmÓí northe lbp genecausehybridsteri|ity.Thesing|enuc|eotide po|ymorphisms(SNPs)we havefound,was usedfor the hap|oýpeana|ysisof the HsÍíregion.
Male infertility and DNA germ cell breaks affected by the epigenetic factor PRDM9
Kusari, Fitore ; Trachtulec, Zdeněk (advisor) ; Děd, Lukáš (referee) ; Liška, František (referee)
DNA-binding histone-3-lysine-4,36-trimethyltransferase PRDM9 specifies meiotic recombination hotspots in mice, rats and humans. Interallelic variation at the Prdm9 locus plays a role in hybrid male sterility. Sterile mouse F1 hybrid male offspring from the PWD × C57BL/6J (B6) cross exhibit meiosis breakdown reminiscent of that observed in Prdm9-deficient B6 sterile mice. However, reciprocal (B6 × PWD)F1 hybrids and some rodent models lacking PRDM9, i.e., PWD and SHR rat males execute meiotic recombination, produce sperm, raising the possibility that PRDM9's role may extend beyond meiosis. Here I demonstrate that PRDM9 is important for post- meiotic male gamete development and release. Unlike their parents, (B6 × PWD)F1 generated spermatozoa of lower quantity and motility but higher percentage of deformations, thus resembling oligoasthenoteratozoospermic (OAT) (semi)sterile men. Histopathological and (ultra)structural analysis revealed compromised spermiogenesis characterized by acrosome detachment and aberrant nucleus elongation in (B6 × PWD)F1 hybrids. Consequently, F1 spermatozoa had malformed acrosomes and nuclear DNA breaks with elevated base oxidation. While deletion of one Prdm9 copy improved sperm phenotypes in (B6 × PWD)F1, copy number gains of the surrounding genes had the opposite effect....
Meiosis and fertility of juvenile mouse males
Valtrová, Pavlína ; Trachtulec, Zdeněk (advisor) ; Reifová, Radka (referee)
This work is a summary of literature on pecularities of spermatogenesis in juvenile mouse males (Mus musculus) and their utilization. Spermatogenesis is a process that leads through meiosis to sperm production. The cell undergoes in waves the following cell types: spermatogonia, spermatocytes, spermatids, and spermatozoa. Juvenile mice (whose testes size and sperm count have not reached their maximum) are often used to study individual cell types. The transition between cell types takes shorter time in juveniles. Spermatozoa from the 1st wave of spermatogenesis (WS) are derived from prenatal gonocytes, allowing earlier sperm production. They have a lower frequency of crossing over (CO rate) due to a different processing of CO intermediates; the consequence can be aneuploidy (one chromosome less/more). Spermatozoa from the 2nd WS still display lower CO rate. In 3rd WS testes descend and their temperature decreases to 33řC; CO rate is more like in adults. In 4th WS is typical testicular supportive cells mature and CO rate is similar to adult levels. Juvenile males also suffer from more frequent and severe sperm malformations. Low CO rate should not have an impact on fertility; errors are eliminated during meiotic checkpoints. However, the children of young fathers have a higher risk of aneuploidy,...

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