Regulation Effect of Different Water Supply to the Nitrogen and Carbon Metabolism

Drought stress and flood result in the generation and accumulation of active oxygen species, the peroxidation of membrane lipids, and reduction of nitrogen metabolism, photosynthesis, growth, and development, causing a significant decline in the qualitative and quantitative production. The water availability influences the different component of NUE and photosynthetic system and its connections. The goal of this chapter is to summarize the effect of water supply to the nitrogen and carbon metabolisms. Knowing about the value of nitrogen use efficiency and photosynthetic parameters is really a useful essential for selecting and growing the best genotypes. But what will happen with these two crucial characteristics of plants, if the environment for growing is not ideal?

DNA repair synthesis and histone deposition partner during homologous recombination

Chromatin remodeling is critical for the regulation of the DNA damage response. We highlight findings from our recent study showing that the deposition of the histone variant H3.3 by the alpha-thalassemia mental retardation X-linked protein (ATRX) and the death domain associated protein (DAXX) chromatin remodeling complex regulates DNA repair synthesis during homologous recombination

ATRX and RECQ5 define distinct homologous recombination subpathways

Homologous recombination (HR) is an important DNA double-strand break (DSB) repair pathway that copies sequence information lost at the break site from an undamaged homologous template. This involves the formation of a recombination structure that is processed to restore the original sequence but also harbors the potential for crossover (CO) formation between the participating molecules. Synthesis-dependent strand annealing (SDSA) is an HR subpathway that prevents CO formation and is thought to predominate in mammalian cells. The chromatin remodeler ATRX promotes an alternative HR subpathway that has the potential to form COs. Here, we show that ATRX-dependent HR outcompetes RECQ5-dependent SDSA for the repair of most two-ended DSBs in human cells and leads to the frequent formation of COs, assessed by measuring sister chromatid exchanges (SCEs). We provide evidence that subpathway choice is dependent on interaction of both ATRX and RECQ5 with proliferating cell nuclear antigen. We also show that the subpathway usage varies among different cancer cell lines and compare it to untransformed cells. We further observe HR intermediates arising as ionizing radiation (IR)-induced ultra-fine bridges only in cells expressing ATRX and lacking MUS81 and GEN1. Consistently, damage-induced MUS81 recruitment is only observed in ATRX-expressing cells. Cells lacking BLM show similar MUS81 recruitment and IR-induced SCE formation as control cells. Collectively, these results suggest that the ATRX pathway involves the formation of HR intermediates whose processing is entirely dependent on MUS81 and GEN1 and independent of BLM. We propose that the predominant ATRX-dependent HR subpathway forms joint molecules distinct from classical Holliday junctions

The DNA-binding box of human SPARTAN contributes to the targeting of Poleta to DNA damage sites

Inappropriate repair of UV-induced DNA damage results in human diseases such as Xeroderma pigmentosum (XP), which is associated with an extremely high risk of skin cancer. A variant form of XP is caused by the absence of Poleta, which is normally able to bypass UV-induced DNA lesions in an error-free manner. However, Poleta is highly error prone when replicating undamaged DNA and, thus, the regulation of the proper targeting of Poleta is crucial for the prevention of mutagenesis and UV-induced cancer formation. Spartan is a novel regulator of the damage tolerance pathway, and its association with Ub-PCNA has a role in Poleta targeting; however, our knowledge about its function is only rudimentary. Here, we describe a new biochemical property of purified human SPARTAN by showing that it is a DNA-binding protein. Using a DNA binding mutant, we provide in vivo evidence that DNA binding by SPARTAN regulates the targeting of Poleta to damage sites after UV exposure, and this function contributes highly to its DNA-damage tolerance function

A tudomány színre lép.: Természettudományos ismeretek óvodásoknak

How a person’s affinity for natural sciences will be depends significantly on what experiences they have in their early childhood. Is it possible to teach science to preschoolers? Yes, if we do it playfully. Small children are generally very open to experimentation and playful exploration. They are happy to set up hypotheses, which are confirmed or refuted by the experiment carried out. In our article, we present experiments and games related to natural sciences and mathematics, which can be adapted to the requirements set out in the kindergarten education program.Az, hogy milyen lesz egy ember természettudományok iránti affinitása, jelentősen függ attól, hogy milyen élmények érik kisgyermekkorában. Lehetséges a természettudomány oktatása óvodásoknak? Igen, ha játékosan csináljuk. A kisgyermekek általában nagyon nyitottak a kísérletezésre, a játékos megismerésre. Szívesen állítanak fel hipotéziseket, melyeket igazol vagy cáfol az elvégzett kísérlet. Tanulmányunkban olyan, a természettudományokhoz és a matematikához kapcsolódó kísérleteket, játékokat mutatunk be, melyek jól illeszthetők az óvodai nevelési programban megfogalmazott követelményekhez

The PCNA-associated protein PARI negatively regulates homologous recombination via the inhibition of DNA repair synthesis

Successful and accurate completion of the replication of damage-containing DNA requires mainly recombination and RAD18-dependent DNA damage tolerance pathways. RAD18 governs at least two distinct mechanisms: translesion synthesis (TLS) and template switching (TS)-dependent pathways. Whereas TS is mainly error-free, TLS can work in an error-prone manner and, as such, the regulation of these pathways requires tight control to prevent DNA errors and potentially oncogenic transformation and tumorigenesis. In humans, the PCNA-associated recombination inhibitor (PARI) protein has recently been shown to inhibit homologous recombination (HR) events. Here, we describe a biochemical mechanism in which PARI functions as an HR regulator after replication fork stalling and during double-strand break repair. In our reconstituted biochemical system, we show that PARI inhibits DNA repair synthesis during recombination events in a PCNA interaction-dependent way but independently of its UvrD-like helicase domain. In accordance, we demonstrate that PARI inhibits HR in vivo, and its knockdown suppresses the UV sensitivity of RAD18-depleted cells. Our data reveal a novel human regulatory mechanism that limits the extent of HR and represents a new potential target for anticancer therapy