Epigenetic dysregulation from chromosomal transit in micronuclei [DLD-1 ATAC-seq]

Default Boolean Operator: Terms in a search string will be connected by the AND operator, EXAMPLE: searching genomic melanoma will produce the same results as genomic AND melanoma .
AND, OR, NOT: Combine terms in a search with the boolean operators AND (to add specificity), OR (to broaden), or NOT (to eliminate a term). Operators must be capitalized (all other search terms are not case-sensitive).
Wild Card: Add wild card symbols * (open-ended) and ? (single character) to truncate terms. EXAMPLE: searching gen* shows results for 'gene', 'genetic', 'genomic, etc. Searching gene? returns results for 'gene' or 'genes' but not for 'genome'.
Phrase Searching: Enclose search in quotation marks "keyword or search term" to search for an exact phrase. EXAMPLE: "transcription factors" returns results for records where transcription is immediately followed by the word factors .
Diacritics: Words containing diacritics translate those characters to non-diacritic form. EXAMPLE: massague returns results for Massague&#769 .
Filter by: Located on the homepage (left panel), use filters to search for records or narrow the search. From search results page, filters can be removed by clicking on the term at the top of the page.

UID: 11145

Author(s): Dameracharla, Bhargavi, Ly, Peter

Description: Summary from GEO:

"Chromosomal instability (CIN) and epigenetic reprograming are characteristic of advanced and metastatic human cancers, yet whether they are mechanistically linked is unknown. Here we show that missegregation of mitotic chromosomes, their sequestration in micronuclei, and subsequent micronuclear envelope rupture significantly disrupt normal histone post-translational modifications, a phenomenon conserved across humans and mice as well as cancer and non-transformed cells. Mislocalization of missegregating chromosomes during anaphase promotes loss of Histone H2B ubiquitination enrichment of histone H3 trimethylation, whereas micronuclear rupture engenders loss of histone H3 acetylation and histone H2A ubiquitination. Using fluorescence lifetime imaging, ATAC-see, and ATAC-seq we show that micronuclei exhibit profound differences in chromatin accessibility. Additionally, chromosomes that are reincorporated into the primary nucleus after transient encapsulation in micronuclei exhibit durable epigenetic dysregulation. Thus, in addition to genomic copy number alterations, CIN can serve as a vehicle for stochastic epigenetic reprogramming and heterogeneity in cancer."

Overall design from GEO:

"ATAC-Seq of single cell clones DLD-1 cells that mis-segregates only the Y-chromosomes and their parental control The colones obtained from CEN-SELECT strategy from Ly et al., Nat. Genet. 2019."

Subject of Study

Subject(s)

Do you have or know of a dataset that should be added to the catalog? Let us know!