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Illuminating the cycle of life
Published in Raquel Seruca, Jasjit S. Suri, João M. Sanches, Fluorescence Imaging and Biological Quantification, 2017
Anabela Ferro, Patrícia Carneiro, Maria Sofia Fernandes, Tânia Mestre, Ivan Sahumbaiev, João M. Sanches, Raquel Seruca
The cell cycle consists of three gap phases, G0, G1, and G2, which are interspersed between the DNA synthesis phase (S phase) and the mitosis phase (M phase). The G0/G1, S, and G2 phases are collectively known as interphase. The cell cycle is a coordinated network of genes and proteins, cyclically regulated by transcription, posttranslational modifications, as well as dynamic genetic and protein interactions [8,9]. Key regulatory molecules include the cyclin-dependent kinases (CDK), a family of serine/threonine kinases that are specifically activated at different phases of the cell cycle by cyclins. Cell-cycle progression is driven by the periodic oscillation of CDK/cyclin activities, which are in turn regulated by a number of mechanisms, including (1) cyclin synthesis; (2) activation of CDKs by CDK activating kinases (CAKs); (3) inhibition of CDKs by CDK inhibitors (CKIs); and (4) ubiquitin-mediated proteasomal degradation of cyclins [9]. Indeed, protein degradation plays a key role in driving cell-cycle transitions through two major E3 ubiquitin ligases, the Skp1–Cul1-F box protein (SCF) complex and the anaphase-promoting complex/cyclosome (APC/C), which ubiquitinate G1 cyclins from late G1 to early M phase and mitotic cyclins from anaphase till the end of G1 phase, respectively [9,10]. Further regulation is accomplished by a myriad of cell-cycle checkpoints that induce cell-cycle arrest on detection of defects and ensure the progression of the cycle in an orderly fashion while minimizing genomic instability [11,12]. Briefly, the G1/S checkpoint induces an arrest induced by DNA damage in a p53-dependent manner, whereas the S phase checkpoint delays initiation or elongation of DNA replication to minimize replications errors. The G2/M checkpoint restricts entry into mitosis minimizing chromosome missegregation, whereas the spindle assembly checkpoint (SAC) detects improper alignment of chromosomes on the mitotic spindle thus ensuring fidelity of chromosome segregation. Finally, postmitotic arrest prevents abnormal daughter cells from entering the next interphase [2,12]. A schematic representation of the cell cycle is displayed in Figure 12.1.
Embryotoxic effects of Rovral® for early chicken (Gallus gallus) development
Published in Journal of Toxicology and Environmental Health, Part A, 2021
Beatriz Mitidiero Stachissini Arcain, Maria Cláudia Gross, Danúbia Frasson Furtado, Carla Vermeulen Carvalho Grade
Both MN and nuclear alterations have been employed as indicators of exposure to genotoxic substances (Ngan et al. 2007). The erythrocytes of birds remain nucleated throughout life (Bellairs and Osmond 2014), and since pesticides induce DNA damage or alter the nuclear structure (Bouaziz et al. 2020), these cells represent a reliable model for these analyses. Treatment with Rovral® at a concentration of 300 µl/ml produced no significant changes in the frequencies of MN and most nuclear abnormalities, as previously reported for reptile (Schaumburg et al. 2016), bird (Conceição and Protti 2012) and fish (Mitkovska and Chassovnikarova 2020) embryos. Nonetheless, a significant increase in binucleated erythrocytes was found. These cells appear in events of aneuploidy, induced by incorrect chromosome segregation (Shi and King 2005). Data indicated that Rovral® did not exert a potent genotoxic effect, as there was little induction of nuclear alterations in erythrocytes. However, experiments were performed with only one concentration and the small sample size used for these analyzes (n = 28) may have affected the results, requiring further studies to conclude the safety of this fungicide.