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Series GSE246986 Query DataSets for GSE246986
Status Public on May 31, 2024
Title Ki67-mediated chromatin accessibility impedes B-cell antigen-receptor gene rearrangement
Organism Mus musculus
Experiment type Genome binding/occupancy profiling by high throughput sequencing
Summary B and T cells can recognise and respond to a vast array of foreign pathogens by virtue of the diverse antigen-receptor repertoire generated by gene rearrangement during development. Here, we show that deficiency in Ki67, a nuclear protein ubiquitously expressed throughout the cell cycle, impairs B-cell development at specific, early stages. We identified that Ki67 maintains global chromatin accessibility in lymphocyte progenitors at stages where antigen-receptor gene rearrangements occur and that gene rearrangement is less efficient in the absence of Ki67. That the defects in B cell development are caused by disrupted antigen-receptor gene rearrangement is shown by pre-rearranged antigen-receptor genes fully compensating for loss of Ki67. Collectively, these results identify a unique contribution from Ki67 to somatic antigen-receptor gene rearrangement.
Overall design B cell progenitors(pre-pro-B, pro-B and small pre-B) were sorted and ATAC-sequencing were performed on these cell populations from WT or Mki67-/- mice
Contributor(s) Ding Z, Hagan M, Yan F, Tarlinton D
Citation(s) 38842525
Submission date Nov 03, 2023
Last update date Jun 12, 2024
Contact name Zhoujie Ding
Organization name Monash University
Street address 89 Commercial Road
City Melbourne
State/province VIC
ZIP/Postal code 3004
Country Australia
Platforms (1)
GPL24247 Illumina NovaSeq 6000 (Mus musculus)
Samples (24)
GSM7881784 WT Pre-pro-B 1
GSM7881785 WT Pre-pro-B 2
GSM7881786 WT Pre-pro-B 3
BioProject PRJNA1035491

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GSE246986_RAW.tar 1.9 Gb (http)(custom) TAR (of BW, NARROWPEAK)
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Raw data are available in SRA

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