Differences in spatial localization and chromatin pattern during different phases of cell cycle between normal and cancer cells

Abstract

We studied differences in chromatin patterns and the spatial localization of centromeres of chromosome 11 during the cell cycle between normal peripheral blood lymphocytes (PBL) and human promyclocytic leukemia cells (HL‐60) using fluorescence in situ hybridization. The pericentromeres in both cells were located at the periphery during Gq (quiescent) phase, but moved towards the nuclear center in G1 and mid‐S phase. During G2, the pericentromeres of PBL continued to move towards the nuclear center whereas those of HL‐60 returned to the periphery. The angle defining the spatial location of two pericentromeres, in reference to the center of the nucleus, increased in PBL cells from a mean of 67° during Gq phase to 106° during G1 phase (P < 0.01), and the two pericentromeres remained wide apart throughout the entire cell cycle. In HL‐60, the angle also increased during G1, but then decreased during mid‐S and G2 phases. Both cells exhibited pericentromeric signals during Gq that were round and compact, and the entire chromatin was loosely condensed. The signal became more loose and dispersed during the G1 and mid‐S phases. The pericentromere signal varied during G2 and was generally rod‐like or bipartite with condensation of the entire chromatin or chromosome‐like. Our results suggest that subtle but important differences in spatial localization of pericentromeres are present during the interphase between normal PBL and HL‐60 cells. Cytometry 27:327–335, 1997. © 1997 Wiley‐Liss, Inc.

Intranuclear relocation of the Plc β 3 sequence in cerebellar Purkinje neurons: temporal association with de novo expression during development

“…Changes in this spatial organization have been postulated to represent one level of control of gene expression by placing actively transcribed genes at transcriptionally competent nuclear sites (De Boni and Mintz 1986;De Boni 1998, 1999;Martou and De Boni 2000). These premises have been supported by evidence that demonstrates spatial rearrangements of chromatin domains in association with pathological states (Borden and Manuelidis 1988;Haaf and Schmid 1989;Tagawa et al 1997) and with conditions that alter transcriptional demands (Holowacz and De Boni 1991;Billia et al 1992;Janevski et al 1995). In support of the latter, specific, actively transcribed sequences have been reported to be positioned more peripherally within chromosome territories than their inactive homologs (Dietzel et al 1999).…”