Please use this identifier to cite or link to this item: https://olympias.lib.uoi.gr/jspui/handle/123456789/38991
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dc.contributor.authorTsomakian, Konstantinosen
dc.contributor.authorΤσομακιάν, Κωνσταντίνοςel
dc.date.accessioned2025-06-02T07:41:13Z-
dc.date.available2025-06-02T07:41:13Z-
dc.identifier.urihttps://olympias.lib.uoi.gr/jspui/handle/123456789/38991-
dc.rightsAttribution-NonCommercial-NoDerivs 3.0 United States*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/3.0/us/*
dc.subjectNuclear Envelopeen
dc.subjectChromatinel
dc.titleNuclear Envelope: protein Interactions and chromatin landscape.en
dc.typemasterThesisen
heal.typemasterThesisel
heal.type.enMaster thesisen
heal.type.elΜεταπτυχιακή εργασίαel
heal.classificationStudy of chromatin organization and dynamics upon loss of A type lamins and lamin B Receptoren
heal.dateAvailable2025-06-02T07:42:14Z-
heal.languageenel
heal.accessfreeel
heal.recordProviderΠανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών Υγείαςel
heal.publicationDate2025-02-27-
heal.abstractIn eukaryotic cells a dual membrane system separates the genetic information stored inside the cell nucleus from the rest of the cell. Wrapped around protein complexes, DNA takes the form of chromatin that can be divided into two main categories, active chromatin and inactive chromatin. In most eukaryotic cells active chromatin, also referred as euchromatin takes up the nuclear interior, while inactive chromatin also referred as heterochromatin takes up the nuclear periphery. Experiments by Salovei et al., have yielded two major findings regarding chromatin organization. First, the two key players responsible for tethering heterochromatin to the nuclear periphery are Lamin B Receptor (LBR) and A type lamins, as downregulation of these proteins leads to a reversed chromatin architecture. Second, this role of LBR and A type lamins is sequential with regards to development as LBR is mostly responsible for heterochromatin tethering to the nuclear periphery during early developmental stages, while A type lamins are responsible for heterochromatin tethering to the nuclear periphery on differentiated cells. Here, we used NIH/3T3 cells, generated by former lab members, where LBR or LMNA/C or both were deleted. Double KO clones were derived from LMNA/C KO cells as well as from LBR KO cells to account for the sequential manner that the two proteins function. We demonstrate that despite the mislocalization of several nuclear envelope proteins, nuclear integrity is maintained in cells lacking both LBR and LMNA/C. Our findings also suggest that the previously reported growth impairment is unlikely to be linked to LBR’s sterol reductase activity. Moreover, while chromatin retains a generally conventional architecture, we observe a subtle shift toward an inverted-like configuration, accompanied by significant changes in gene expression and modest alterations in chromatin dynamics. The maintenance of conventional chromatin organization in the absence of these key envelope components points to the involvement of additional mechanisms governing chromatin topology. Furthermore, given the lack of compelling evidence implicating LBR or LMNA/C in specific biological processes, we support the prevailing view that these proteins primarily serve as general-purpose chromatin tethers rather than functioning in specialized cellular pathways. Finally, we successfully established stable cell lines for future identification of potential PRR14 and LBR interactors, as well as the local proteome environment of these proteins, using the BioID2 proximity labeling system.en
heal.advisorNamePolitou, Anastasiaen
heal.committeeMemberNamePolitou, Anastasiaen
heal.committeeMemberNameΠολίτου, Αναστασίαel
heal.committeeMemberNamePapamarkaki, Thomaisen
heal.committeeMemberNameΠαπαμαρκάκη, Θωμαΐςel
heal.committeeMemberNameLiakopoulos, Dimitriosen
heal.committeeMemberNameΛιακόπουλος, Δημήτριοςel
heal.committeeMemberNameGeorgatos, Spiridonen
heal.committeeMemberNameΓεωργάτος, Σπυρίδωνel
heal.committeeMemberNameFriligos, Efstathiosen
heal.committeeMemberNameΦριλίγγος, Ευστάθιοςel
heal.academicPublisherΠανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών Υγείας. Τμήμα Ιατρικήςel
heal.academicPublisherIDuoiel
heal.numberOfPages114el
heal.fullTextAvailabilitytrue-
Appears in Collections:Διατριβές Μεταπτυχιακής Έρευνας (Masters) - ΙΑΤ

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