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Natarajan Chandrasekaran - One of the best experts on this subject based on the ideXlab platform.
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genotoxicity of silver nanoparticles in allium cepa
Science of The Total Environment, 2009Co-Authors: Mamta Kumari, Amitava Mukherjee, Natarajan ChandrasekaranAbstract:Abstract Potential health and environmental effects of nanoparticles need to be thoroughly assessed before their widespread commercialization. Though there are few studies on cytotoxicity of nanoparticles on mammalian and human cell lines, there are hardly any reports on genotoxic and cytotoxic behavior of nanoparticles in plant cells. This study aims to investigate cytotoxic and genotoxic impacts of silver nanoparticles using root tip cells of Allium cepa as an indicator organism. A. cepa root tip cells were treated with four different concentrations (25, 20, 75, and 100 ppm) of engineered silver nanoparticles (below 100 nm size) dispersion, to study endpoints like mitotic index, distribution of cells in mitotic phases, different types of chromosomal aberrations, disturbed metaphase, sticky chromosome, cell wall disintegration, and breaks. For each concentration five sets of microscopic observations were carried out. No chromosomal aberration was observed in the control (untreated onion root tips) and the mitotic index (MI) value was 60.3%. With increasing concentration of the nanoparticles decrease in the mitotic index was noticed (60.30% to 27.62%). The different cytological effects including the chromosomal aberrations were studied in detail for the treated cells as well as control. We infer from this study that silver nanoparticles could penetrate plant system and may impair stages of cell division causing Chromatin Bridge, stickiness, disturbed metaphase, multiple chromosomal breaks and cell disintegration. The findings also suggest that plants as an important component of the ecosystems need to be included when evaluating the overall toxicological impact of the nanoparticles in the environment.
Mathieu Sicard - One of the best experts on this subject based on the ideXlab platform.
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CI embryos from infected fathers and uninfected mothers: An arrest after the first nuclear divisions.
2018Co-Authors: Manon Bonneau, Frédéric Landmann, Pierrick Labbé, Fabienne Justy, Mylène Weill, Mathieu SicardAbstract:Paternal Chromatin appears in green/yellow (acetylated histone H4 labelling is dominant) and maternal Chromatin appears in red (propidium iodide labelling is dominant) (A) apposition of maternal and paternal pronuclei, (B) paternal Chromatin failed to segregate and form a Chromatin Bridge between segregated maternal Chromatin, (C) two nuclei containing mainly maternal Chromatin while paternal Chromatin do not segregate, (D) abnormal development at 2 hours after oviposition: only few aborted divisions are observed, (E) none of the embryos from such crosses exhibited any visible development under microscope 48 hours post-oviposition. White arrows indicate the paternal Chromatin. Confocal stacks (panels A,B,C,D,) and optical images (panels E) were obtained on embryos from several CI crosses between infected males and uninfected females due to the difficulty to obtain all the early embryonic stages for each cross (S2 Table). Green dots are background noises likely due to the presence of residual antibodies. Scale bar is 10μm.
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CI embryos from incompatible infected parents in C. pipiens: From first nuclear divisions to segmentation.
2018Co-Authors: Manon Bonneau, Frédéric Landmann, Pierrick Labbé, Fabienne Justy, Mylène Weill, Mathieu SicardAbstract:Paternal Chromatin appears in green/yellow (acetylated histone H4 labelling is dominant) and maternal Chromatin appears in red (propidium iodide labelling is dominant) (A) apposition of maternal and paternal pronuclei, (B) delay in paternal Chromatin condensation, (C) condensed maternal Chromatin and under-condensed paternal Chromatin, (D) paternal Chromatin failed to segregate and form a Chromatin Bridge between segregating maternal Chromatin, (E) two nuclei containing mainly maternal Chromatin while paternal Chromatin do not segregate, (F) haploid development 2 hours after oviposition, (G) the two possible fates of development after 48 hours (1) non-viable embryo with no visible development, and (2) unhatched developed embryo with visible segments. White arrows indicate the paternal Chromatin. Confocal stacks (panels A,B,C,D,E,F) and optical images (panels G1 and G2) were obtained on embryos from several CI crosses between infected males and females due to the difficulty to obtain all the early embryonic stages for each cross (S2 Table). Green dots are background noises likely due to the presence of residual antibodies. Scale bar is 10μm.
Mamta Kumari - One of the best experts on this subject based on the ideXlab platform.
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genotoxicity of silver nanoparticles in allium cepa
Science of The Total Environment, 2009Co-Authors: Mamta Kumari, Amitava Mukherjee, Natarajan ChandrasekaranAbstract:Abstract Potential health and environmental effects of nanoparticles need to be thoroughly assessed before their widespread commercialization. Though there are few studies on cytotoxicity of nanoparticles on mammalian and human cell lines, there are hardly any reports on genotoxic and cytotoxic behavior of nanoparticles in plant cells. This study aims to investigate cytotoxic and genotoxic impacts of silver nanoparticles using root tip cells of Allium cepa as an indicator organism. A. cepa root tip cells were treated with four different concentrations (25, 20, 75, and 100 ppm) of engineered silver nanoparticles (below 100 nm size) dispersion, to study endpoints like mitotic index, distribution of cells in mitotic phases, different types of chromosomal aberrations, disturbed metaphase, sticky chromosome, cell wall disintegration, and breaks. For each concentration five sets of microscopic observations were carried out. No chromosomal aberration was observed in the control (untreated onion root tips) and the mitotic index (MI) value was 60.3%. With increasing concentration of the nanoparticles decrease in the mitotic index was noticed (60.30% to 27.62%). The different cytological effects including the chromosomal aberrations were studied in detail for the treated cells as well as control. We infer from this study that silver nanoparticles could penetrate plant system and may impair stages of cell division causing Chromatin Bridge, stickiness, disturbed metaphase, multiple chromosomal breaks and cell disintegration. The findings also suggest that plants as an important component of the ecosystems need to be included when evaluating the overall toxicological impact of the nanoparticles in the environment.
Δανδουλάκη Μαρία - One of the best experts on this subject based on the ideXlab platform.
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Chk1 and Src proteins prevent Chromatin Bridge breakage in cytokinesis
Πανεπιστήμιο Κρήτης, 2018Co-Authors: Dandoulaki Maria, Δανδουλάκη ΜαρίαAbstract:Chromatin Bridges are DNA strings of incompletely segregated Chromatin which connect the daughter nuclei during cytokinesis. If unresolved, Chromatin Bridges can be fragmented during furrow ingression in cytokinesis, leading to genetic instability. The presence of Chromatin Bridges activates the abscission checkpoint which in turn delays the final cut of the cytoplasm, thus protecting from DNA Bridge breakage. Furthermore, actin-rich structures known as actin patches, are formed at the base of the Chromatin Bridge. It has been suggested that under normal conditions, the actin patches stabilize the intercellular canal until the DNA Bridge is resolved. Though, how actin patches are formed remains largely enigmatic. The nonreceptor tyrosine kinase Src, has been implicated in the rearrangement of actin cytoskeleton. In the present study, we have shown that in human cells, Src inhibition leads to increased Chromatin Bridge breakage and elevated frequency of cells exhibiting micronuclei. However, DNA Bridge breakage in Chk1- or Src-deficient cells correlates with reduced actin patches at the bases of Chromatin Bridges and is not caused by abscission. Activated Src is localized to the actin patches at the bases of DNA Bridges during cytokinesis. Additionally, Chk1 downregulation results in reduced Src activity, loss of actin patches and increased DNA Bridge breakage. Furthermore, we found that Chk1 phosphorylates Src at a newly identified site, Serine 51, and that phosphorylation is required to fully induce Src kinase activity. Phosphorylated Src at Serine 51 is localized at the bases of DNA Bridges, at the cellular membrane and the nucleus. Mutation of Serine 51 to the non-phosphorylatable aminoacid Alanine, leads to reduced actin patches and increased DNA Chromatin breakage, whereas expression of a phosphomimicking Src-S51D protein rescues actin patches and prevents Chromatin breakage in Chk1-deficient cells. Based on these results, we suggest a novel mechanism required for stabilization of DNA Bridges during cytokinesis, which involves Chk1- and Src- dependent formation of actin patches at the bases of Chromatin Bridges.Οι γέφυρες χρωματίνης είναι νήματα DNA τα οποία ενώνουν τους θυγατρικούς πυρήνες κατά το τέλος της κυτταροκίνησης και, εάν δεν επιλυθούν, μπορούν να σπάσουν προκαλώντας χρωμοσωμική αστάθεια. Παρουσία γεφυρών χρωματίνης ενεργοποιείται το abscission checkpoint το οποίο καθυστερεί το τελικό κόψιμο του κυτταροπλάσματος, για να μη σπάσουν οι γέφυρες χρωματίνης. Ακόμη, εκατέρωθεν των χρωματινικών γεφυρών σχηματίζονται δομές ακτίνης (actin patches), οι οποίες στα φυσιολογικά κύτταρα σταθεροποιούν τις γέφυρες DNA έως ότου αυτές επιλυθούν. Ωστόσο, ο μηχανισμός δημιουργίας των actin patches δεν έχει ακόμα βρεθεί. Η πρωτεϊνική κινάση τυροσίνης Src, συμμετέχει στην αναδιοργάνωση του κυτταροσκελετού. Στην παρούσα μελέτη, δείξαμε ότι αναστολή της Src σε κύτταρα ανθρώπου οδηγεί σε αύξηση του ποσοστού των σπασμένων γεφυρών DNA στην κυτταροκίνηση και αύξηση του ποσοστού των κυττάρων με μικροπυρήνες. Ωστόσο, το σπάσιμο των γεφυρών DNA σε κύτταρα χωρίς λειτουργική Chk1 ή Src συσχετίζεται με απώλεια των actin patches στις βάσεις των γεφυρών DNA και όχι με δυσλειτουργία του abscission checkpoint. Η ενεργοποιημένη πρωτεΐνη Src εντοπίζεται στα actin patches, στις βάσεις των γεφυρών DNA στην κυτταροκίνηση. Επίσης, μείωση της κινάσης Chk1 οδηγεί σε μείωση της ενεργότητας της πρωτεΐνης Src, απώλεια των actin patches και αύξηση του ποσοστού των σπασμένων γεφυρών DNA στην κυτταροκίνηση. Ακόμη, δείξαμε ότι η Chk1 φωσφορυλιώνει την πρωτεΐνη Src σε μία νέα θέση, τη Σερίνη 51 και ότι η φωσφορυλιωμένη Src στη Σερίνη 51 εντοπίζεται στις βάσεις των γεφυρών DNA, την κυτταρική μεμβράνη και τον πυρήνα. Η φωσφορυλίωση της Src στη Σερίνη 51 απαιτείται για πλήρη ενεργοποίηση της Src. Έκφραση της μεταλλαγμένης Src S51A, στην οποία η Σερίνη 51 έχει μεταλλαχθεί σε Αλανίνη ώστε η θέση αυτή να μη φωσφορυλιώνεται in vivo, οδηγεί σε μείωση του ποσοστού των γεφυρών DNA με actin patches και αύξηση του ποσοστού των σπασμένων γεφυρών DNA. Αντίθετα, έκφραση της μεταλλαγμένης Src S51D, όπου η Σερίνη 51 έχει μεταλλαχθεί σε Ασπαραγινικό οξύ ώστε η θέση αυτή να μιμείται συνεχώς την φωσφορυλίωση, προστατεύει την δημιουργία των actin patches και εμποδίζει το σπάσιμο των γεφυρών DNA σε κύτταρα με μειωμένη έκφραση των Chk1 και Src πρωτεϊνών. Με βάση τα δεδομένα αυτά, προτείνουμε ένα νέο μηχανισμό σταθεροποίησης των γέφυρων DNA κατά την κυτταροκίνηση, μέσω διατήρησης των actin patches από τις πρωτείνες Chk1 και Src
George Zachos - One of the best experts on this subject based on the ideXlab platform.
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Src activation by Chk1 promotes actin patch formation and prevents Chromatin Bridge breakage in cytokinesis.
Journal of Cell Biology, 2018Co-Authors: Maria Dandoulaki, Eleni Petsalaki, David Sumpton, Sara Zanivan, George ZachosAbstract:In cytokinesis with Chromatin Bridges, cells delay abscission and retain actin patches at the intercellular canal to prevent chromosome breakage. In this study, we show that inhibition of Src, a protein-tyrosine kinase that regulates actin dynamics, or Chk1 kinase correlates with Chromatin breakage and impaired formation of actin patches but not with abscission in the presence of Chromatin Bridges. Chk1 is required for optimal localization and complete activation of Src. Furthermore, Chk1 phosphorylates human Src at serine 51, and phosphorylated Src localizes to actin patches, the cell membrane, or the nucleus. Nonphosphorylatable mutation of S51 to alanine reduces Src catalytic activity and impairs formation of actin patches, whereas expression of a phosphomimicking Src-S51D protein rescues actin patches and prevents Chromatin breakage in Chk1-deficient cells. We propose that Chk1 phosphorylates Src-S51 to fully induce Src kinase activity and that phosphorylated Src promotes formation of actin patches and stabilizes Chromatin Bridges. These results identify proteins that regulate formation of actin patches in cytokinesis.