RESUMO
We present the formation of quasi-periodic cool spicule-like jets in the solar atmosphere using 2.5-D numerical simulation in two-fluid regime (ions+neutrals) under the presence of thermal conduction and ion-neutral collision. The nonlinear, impulsive Alfvénic perturbations at the top of the photosphere trigger field aligned magnetoacoustic perturbations due to ponderomotive force. The transport of energy from Alfvén pulse to such vertical velocity perturbations due to ponderomotive force is considered as an initial trigger mechanism. Thereafter, these velocity perturbations steepen into the shocks followed by quasi-periodic rise and fall of the cool jets transporting mass in the overlying corona. This article is part of the theme issue 'Partially ionized plasma of the solar atmosphere: recent advances and future pathways'.
RESUMO
The developmental asymmetry of fission yeast daughter cells derives from inheriting 'older Watson' versus 'older Crick' DNA strand from the parental cell, strands that are complementary but not identical with each other. A novel DNA strand-specific 'imprint', installed during DNA replication at the mating-type locus (mat1), imparts competence for cell type inter-conversion to one of the two chromosome replicas. The catalytic subunit of DNA Polymerase α (Polα) has been implicated in the imprinting process. Based on its known biochemical function, Polα might install the mat1 imprint during lagging strand synthesis. The nature of the imprint is not clear: it is either a nick or a ribonucleotide insertion. Our investigations do not support a direct role of Polα in nicking through putative endonuclease domains but confirm its indirect role in installing an alkali-labile moiety as the imprint. While ruling out the role of the primase subunit of Polα holoenzyme, we find that mutations in the Polα-recruitment and putative primase homology domain in Mcm10/Cdc23 abrogate the ribonucleotide imprint formation. These results, while confirming the ribonucleotide nature of the imprint suggest the possibility of a direct role of Mcm10/Cdc23 in installing it in cooperation with Polα and Swi1.
Assuntos
Proteínas de Ciclo Celular/metabolismo , DNA Polimerase I/metabolismo , Replicação do DNA/genética , Genes Fúngicos Tipo Acasalamento/genética , Proteínas de Manutenção de Minicromossomo/metabolismo , Ribonucleotídeos/genética , Proteínas de Schizosaccharomyces pombe/metabolismo , Schizosaccharomyces/genética , Schizosaccharomyces/metabolismo , Domínio Catalítico , Proteínas de Ciclo Celular/química , Proteínas de Ciclo Celular/genética , DNA Polimerase I/química , DNA Polimerase I/genética , DNA Primase/química , DNA Primase/metabolismo , Proteínas de Ligação a DNA/genética , Proteínas de Ligação a DNA/metabolismo , Proteínas de Manutenção de Minicromossomo/química , Proteínas de Schizosaccharomyces pombe/química , Proteínas de Schizosaccharomyces pombe/genéticaRESUMO
The spatial and temporal organization of genome duplication, also referred to as the replication program, is defined by the distribution and the activities of the sites of replication initiation across the genome. Alterations to the replication profile are associated with cell fate changes during development and in pathologies, but the importance of undergoing S phase with distinct and specific programs remains largely unexplored. We have recently addressed this question, focusing on the interplay between the replication program and genome maintenance. In particular, we demonstrated that when cells encounter challenges to DNA synthesis, the organization of DNA replication drives the response to replication stress that is mediated by the ATR/Rad3 checkpoint pathway, thus shaping the pattern of genome instability along the chromosomes. In this review, we present the major findings of our study and discuss how they may bring new perspectives to our understanding of the biological importance of the replication program.
Assuntos
Proteínas de Ciclo Celular/metabolismo , Replicação do DNA , Instabilidade Genômica , Proteínas de Schizosaccharomyces pombe/metabolismo , Schizosaccharomyces/genética , Proteínas de Ciclo Celular/genética , Dano ao DNA , Genoma Fúngico , Fase S , Schizosaccharomyces/metabolismo , Proteínas de Schizosaccharomyces pombe/genética , Transdução de SinaisRESUMO
Progression through the cell cycle is driven by the activities of the cyclin-dependent kinase (CDK) family of enzymes, which establish an ordered passage through the cell cycle phases. CDK activity is crucial for the cellular transitions from G1 to S and G2 to M, which are highly controlled to promote the faithful duplication of the genetic material and the transmission of the genome into daughter cells, respectively. While oscillations in CDK activity are essential for cell division, how its specific dynamics may shape cellular processes remains an open question. Recently, we have investigated the potential role of CDK in establishing the profile of replication initiation along the chromosomes, also referred to as the replication program. Our results demonstrated that the timing and level of CDK activity at G1/S provide two critical and independent inputs that modulate the pattern of origin usage. In this review, we will present the conclusions of our study and discuss the implications of our findings for cellular function and physiology.
Assuntos
Ciclo Celular/fisiologia , Cromossomos Humanos/metabolismo , Quinases Ciclina-Dependentes/metabolismo , Replicação do DNA/fisiologia , Genoma Humano/fisiologia , Animais , HumanosRESUMO
Histone post-translational modifications promote a chromatin environment that controls transcription, DNA replication and repair, but surprisingly few phosphorylations have been documented. We report the discovery of histone H3 serine-57 phosphorylation (H3S57ph) and show that it is implicated in different DNA repair pathways from fungi to vertebrates. We identified CHK1 as a major human H3S57 kinase, and disrupting or constitutively mimicking H3S57ph had opposing effects on rate of recovery from replication stress, 53BP1 chromatin binding, and dependency on RAD52. In fission yeast, mutation of all H3 alleles to S57A abrogated DNA repair by both non-homologous end-joining and homologous recombination, while cells with phospho-mimicking S57D alleles were partly compromised for both repair pathways, presented aberrant Rad52 foci and were strongly sensitised to replication stress. Mechanistically, H3S57ph loosens DNA-histone contacts, increasing nucleosome mobility, and interacts with H3K56. Our results suggest that dynamic phosphorylation of H3S57 is required for DNA repair and recovery from replication stress, opening avenues for investigating the role of this modification in other DNA-related processes.
Assuntos
Histonas , Vírus da Influenza A , Humanos , Animais , Fosforilação , Processamento de Proteína Pós-Traducional , Reparo do DNA , CromatinaRESUMO
Random spore analysis is a fundamental tool of yeast genetics for determining gene linkage and the generation of recombinant progeny by genetic crosses. Experimentally it involves treatment of a mating mix with enzymes, such as zymolyase or lyticase, that selectively lyse the cell wall of vegetative cells rather than the spores. Here, we describe a method whereby the relative refractory nature of the spores to treatment with elevated temperature and repeated freeze-thawing facilitates random spore analysis at low cost in fission yeast Schizosaccharomyces pombe. Because of similar properties of spores in budding yeast, this method should prove to be useful for random spore analysis in both budding and fission yeasts.