After fertilization, remodeling of the oocyte and sperm genome is essential for the successful initiation of mitotic activity in the fertilized oocyte and subsequent proliferative activity of the early embryo. Despite the fact that the molecular mechanisms of cell cycle control in early mammalian embryos are in principle comparable to those in somatic cells, there are differences resulting from the specific nature of the gene totipotency of the blastomeres of early cleavage embryos. In this review, we focus on the Chk1 kinase as a key transduction factor in monitoring the integrity of DNA molecules during early embryogenesis.

• Klíčová slova
• Chk1 kinase, DNA damage, cell cycle checkpoint, cleaving embryo,
• MeSH
• checkpoint kinasa 1 * metabolismus   MeSH
• embryo savčí enzymologie   MeSH
• embryonální vývoj * genetika   MeSH
• poškození DNA * MeSH
• zvířata MeSH
• Check Tag
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• přehledy MeSH
• Názvy látek
• checkpoint kinasa 1 * MeSH

The nuclear pore complex (NPC) facilitates the trafficking of proteins and RNA between the nucleus and cytoplasm. The role of nucleoporins (Nups) in transport in the context of the NPC is well established, yet their function in tRNA export has not been fully explored. We selected several nucleoporins from different parts of the NPC to investigate their potential role in tRNA trafficking in Trypanosoma brucei. We show that while all of the nucleoporins studied are essential for cell viability, only TbNup62 and TbNup53a function in tRNA export. In contrast to homologs in yeast TbNup144 and TbNup158, which are part of the inner and outer ring of the NPC, have no role in nuclear tRNA trafficking. Instead, TbNup144 plays a critical role in nuclear division, highlighting the role of nucleoporins beyond nucleocytoplasmic transport. These results suggest that the location of nucleoporins within the NPC is crucial to maintaining various cellular processes.

• Klíčová slova
• FG-Nups, NPC, Trypanosoma brucei, nuclear division, nucleoporins, tRNA trafficking,
• MeSH
• aktivní transport - buněčné jádro MeSH
• buněčné jádro metabolismus   MeSH
• jaderný pór * genetika   metabolismus   MeSH
• komplex proteinů jaderného póru * genetika   MeSH
• Saccharomyces cerevisiae genetika   metabolismus   MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• komplex proteinů jaderného póru * MeSH

The transition from sexual reproduction to asexuality is often triggered by hybridization. The gametogenesis of many hybrid asexuals involves premeiotic genome endoreplication leading to bypass hybrid sterility and forming clonal gametes. However, it is still not clear when endoreplication occurs, how many gonial cells it affects and whether its rate differs among clonal lineages. Here, we investigated meiotic and premeiotic cells of diploid and triploid hybrids of spined loaches (Cypriniformes: Cobitis) that reproduce by gynogenesis. We found that in naturally and experimentally produced F1 hybrids asexuality is achieved by genome endoreplication, which occurs in gonocytes just before entering meiosis or, rarely, one or a few divisions before meiosis. However, genome endoreplication was observed only in a minor fraction of the hybrid's gonocytes, while the vast majority of gonocytes were unable to duplicate their genomes and consequently could not proceed beyond pachytene due to defects in bivalent formation. We also noted that the rate of endoreplication was significantly higher among gonocytes of hybrids from natural clones than of experimentally produced F1 hybrids. Thus, asexuality and hybrid sterility are intimately related phenomena and the transition from sexual reproduction to asexuality must overcome significant problems with genome incompatibilities with a possible impact on reproductive potential.

• Klíčová slova
• Cobitis taenia complex, endoreplication, gynogenesis, hybrid sterility, meiosis, polyploidy,
• MeSH
• gametogeneze genetika   MeSH
• hybridizace genetická MeSH
• křížení genetické MeSH
• máloostní genetika   růst a vývoj   MeSH
• meióza genetika   MeSH
• nepohlavní rozmnožování genetika   MeSH
• rozmnožování genetika   MeSH
• Taenia genetika   růst a vývoj   MeSH
• zvířata MeSH
• Check Tag
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH

The Aurora protein kinases are well-established regulators of spindle building and chromosome segregation in mitotic and meiotic cells. In mouse oocytes, there is significant Aurora kinase A (AURKA) compensatory abilities when the other Aurora kinase homologs are deleted. Whether the other homologs, AURKB or AURKC can compensate for loss of AURKA is not known. Using a conditional mouse oocyte knockout model, we demonstrate that this compensation is not reciprocal because female oocyte-specific knockout mice are sterile, and their oocytes fail to complete meiosis I. In determining AURKA-specific functions, we demonstrate that its first meiotic requirement is to activate Polo-like kinase 1 at acentriolar microtubule organizing centers (aMTOCs; meiotic spindle poles). This activation induces fragmentation of the aMTOCs, a step essential for building a bipolar spindle. We also show that AURKA is required for regulating localization of TACC3, another protein required for spindle building. We conclude that AURKA has multiple functions essential to completing MI that are distinct from AURKB and AURKC.

• MeSH
• aparát dělícího vřeténka genetika   MeSH
• aurora kinasa A genetika   MeSH
• aurora kinasa B genetika   MeSH
• aurora kinasa C genetika   MeSH
• dělení bunečného jádra genetika   MeSH
• fetální proteiny genetika   MeSH
• lidé MeSH
• meióza genetika   MeSH
• myši MeSH
• oocyty růst a vývoj   metabolismus   MeSH
• organizační centrum mikrotubulů metabolismus   MeSH
• polo-like kinasa 1 MeSH
• póly dělícího vřeténka genetika   MeSH
• protein-serin-threoninkinasy genetika   MeSH
• proteiny asociované s mikrotubuly genetika   MeSH
• proteiny buněčného cyklu genetika   MeSH
• protoonkogenní proteiny genetika   MeSH
• segregace chromozomů genetika   MeSH
• vývojová regulace genové exprese genetika   MeSH
• zvířata MeSH
• Check Tag
• lidé MeSH
• myši MeSH
• ženské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Research Support, N.I.H., Extramural MeSH
• Názvy látek
• Aurkb protein, mouse MeSH Prohlížeč
• Aurkc protein, mouse MeSH Prohlížeč
• aurora kinasa A MeSH
• aurora kinasa B MeSH
• aurora kinasa C MeSH
• fetální proteiny MeSH
• protein-serin-threoninkinasy MeSH
• proteiny asociované s mikrotubuly MeSH
• proteiny buněčného cyklu MeSH
• protoonkogenní proteiny MeSH
• TACC3 protein, mouse MeSH Prohlížeč

The degradation of maternally provided molecules is a very important process during early embryogenesis. However, the vast majority of studies deals with mRNA degradation and protein degradation is only a very little explored process yet. The aim of this article was to summarize current knowledge about the protein degradation during embryogenesis of mammals. In addition to resuming of known data concerning mammalian embryogenesis, we tried to fill the gaps in knowledge by comparison with facts known about protein degradation in early embryos of non-mammalian species. Maternal protein degradation seems to be driven by very strict rules in terms of specificity and timing. The degradation of some maternal proteins is certainly necessary for the normal course of embryonic genome activation (EGA) and several concrete proteins that need to be degraded before major EGA have been already found. Nevertheless, the most important period seems to take place even before preimplantation development-during oocyte maturation. The defects arisen during this period seems to be later irreparable.

• Klíčová slova
• Autophagy, Embryonic genome activation, Maternal to zygotic transition, Proteasome system, Ubiquitin, Ubiquitin ligase,
• MeSH
• embryo nesavčí metabolismus   fyziologie   MeSH
• embryo savčí metabolismus   fyziologie   MeSH
• embryonální vývoj fyziologie   MeSH
• genom fyziologie   MeSH
• lidé MeSH
• oocyty metabolismus   fyziologie   MeSH
• proteiny metabolismus   MeSH
• vývojová regulace genové exprese fyziologie   MeSH
• zvířata MeSH
• Check Tag
• lidé MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• přehledy MeSH
• Názvy látek
• proteiny MeSH

Microtubules, part of the cytoskeleton, are indispensable for intracellular movement, cell division, and maintaining cell shape and polarity. In addition, microtubules play an important role in viral infection. In this review, we summarize the role of the microtubules' network during polyomavirus infection. Polyomaviruses usurp microtubules and their motors to travel via early and late acidic endosomes to the endoplasmic reticulum. As shown for SV40, kinesin-1 and microtubules are engaged in the release of partially disassembled virus from the endoplasmic reticulum to the cytosol, and dynein apparently assists in the further disassembly of virions prior to their translocation to the cell nucleus-the place of their replication. Polyomavirus gene products affect the regulation of microtubule dynamics. Early T antigens destabilize microtubules and cause aberrant mitosis. The role of these activities in tumorigenesis has been documented. However, its importance for productive infection remains elusive. On the other hand, in the late phase of infection, the major capsid protein, VP1, of the mouse polyomavirus, counteracts T-antigen-induced destabilization. It physically binds microtubules and stabilizes them. The interaction results in the G2/M block of the cell cycle and prolonged S phase, which is apparently required for successful completion of the viral replication cycle.

• Klíčová slova
• T antigens, VP1 capsid protein, cell cycle block, dynein, kinesin, microtubules, molecular motors, polyomavirus, virus, virus trafficking,
• MeSH
• buněčné jádro virologie   MeSH
• cytosol virologie   MeSH
• endoplazmatické retikulum virologie   MeSH
• endozomy virologie   MeSH
• interakce hostitele a patogenu * MeSH
• lidé MeSH
• mikrotubuly fyziologie   virologie   MeSH
• myši MeSH
• Polyomavirus genetika   patogenita   MeSH
• replikace viru MeSH
• vazba proteinů MeSH
• virové plášťové proteiny genetika   metabolismus   MeSH
• zvířata MeSH
• Check Tag
• lidé MeSH
• myši MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• přehledy MeSH
• Názvy látek
• virové plášťové proteiny MeSH
• VP1 protein, polyomavirus MeSH Prohlížeč

Chromosome segregation errors are highly frequent in mammalian female meiosis, and their incidence gradually increases with maternal age. The fate of aneuploid eggs is obviously dependent on the stringency of mechanisms for detecting unattached or repairing incorrectly attached kinetochores. In case of their failure, the newly formed embryo will inherit the impaired set of chromosomes, which will have severe consequences for its further development. Whether spindle assembly checkpoint (SAC) in oocytes is capable of arresting cell cycle progression in response to unaligned kinetochores was discussed for a long time. It is known that abolishing SAC increases frequency of chromosome segregation errors and causes precocious entry into anaphase; SAC, therefore, seems to be essential for normal chromosome segregation in meiosis I. However, it was also reported that for anaphase-promoting complex (APC) activation, which is a prerequisite for entering anaphase; alignment of only a critical mass of kinetochores on equatorial plane is sufficient. This indicates that the function of SAC and of cooperating chromosome attachment correction mechanisms in oocytes is different from somatic cells. To analyze this phenomenon, we used live cell confocal microscopy to monitor chromosome movements, spindle formation, APC activation and polar body extrusion (PBE) simultaneously in individual oocytes at various time points during first meiotic division. Our results, using oocytes from aged animals and interspecific crosses, demonstrate that multiple unaligned kinetochores and severe congression defects are tolerated at the metaphase to anaphase transition, although such cells retain sensitivity to nocodazole. This indicates that checkpoint mechanisms, operating in oocytes at this point, are essential for accurate timing of APC activation in meiosis I, but they are insufficient in detection or correction of unaligned chromosomes, preparing thus conditions for propagation of the aneuploidy to the embryo.

• MeSH
• anafáze MeSH
• anafázi podporující komplex MeSH
• aneuploidie MeSH
• časosběrné zobrazování metody   MeSH
• histony genetika   metabolismus   MeSH
• kinetochory metabolismus   MeSH
• komplexy ubikvitinligas genetika   metabolismus   MeSH
• konfokální mikroskopie metody   MeSH
• kontrolní body M fáze buněčného cyklu MeSH
• metafáze MeSH
• mikroinjekce MeSH
• myši inbrední C57BL MeSH
• myši MeSH
• oocyty cytologie   metabolismus   MeSH
• párování chromozomů * MeSH
• proteolýza MeSH
• savčí chromozomy genetika   metabolismus   MeSH
• savci MeSH
• segregace chromozomů * MeSH
• sekurin MeSH
• transportní proteiny genetika   metabolismus   MeSH
• tubulin genetika   metabolismus   MeSH
• zvířata MeSH
• Check Tag
• mužské pohlaví MeSH
• myši MeSH
• ženské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• anafázi podporující komplex MeSH
• histony MeSH
• komplexy ubikvitinligas MeSH
• sekurin MeSH
• transportní proteiny MeSH
• tubulin MeSH