Fluorescence in Situ Hybridization and Human Cell Cycle Genes

1996 ◽  
pp. 29-45
Author(s):  
Douglas J. Demetrick
Keyword(s):  
Cell Cycle ◽  
In Situ Hybridization ◽  
Fluorescence In Situ Hybridization ◽  
Human Cell ◽  
Cell Cycle Genes

scholarly journals Molecular characterization of 12p abnormalities in hematologic malignancies: deletion of KIP1, rearrangement of TEL, and amplification of CCND2

Blood ◽  
1996 ◽  
Vol 87 (1) ◽  
pp. 324-330 ◽  
Author(s):  
M Hoglund ◽  
B Johansson ◽  
J Pedersen-Bjergaard ◽  
P Marynen ◽  
F Mitelman
Keyword(s):  
Cell Cycle ◽  
In Situ Hybridization ◽  
Tumor Suppressor ◽  
Fluorescence In Situ Hybridization ◽  
Hematologic Malignancies ◽  
Suppressor Gene ◽  
Detectable Change ◽  
Structural Rearrangements

Twenty patients with hematologic malignancies with 12p abnormalities were investigated by fluorescence in situ hybridization (FISH) using probes mapped to specific regions in 12p. The initial analysis using the YAC 964c10 (D12S736) revealed that all four cases with cytogenetically identified del(12p) had lost one copy of this YAC and that submicroscopic deletions had occurred in 10 of the 16 neoplasms with other 12p abnormalities, ie, translocations, additions, and insertions. The deletions were partially mapped with cosmids localized to subregions of 12p. One copy of the gene for p27kip1 (KIP1), involved in cell cycle entrance, was found to be lost in all cases in which deletions could be detected by other probes and in one case with a translocation as the only detectable change. This implicates KIP1 as a possible tumor suppressor gene affected by del(12p). Four translocations with no apparent concomitant deletions were detected. All four breakpoints resulted in a split D12S736 signal. In two of these cases, we showed that TEL was disrupted as a result of a t(5;12)(q32–33;p12) and a t(12;22)(p12;q12), respectively. Two lymphoid neoplasm--one non-Hodgkin's lymphoma and one Burkitt's lymphoma--with 12p amplifications were detected. In both cases cyclin D2 (CCND2) was within the amplified region. Thus, cytogenetic abnormalities of 12p in hematologic malignancies result in at least three different molecular changes: deletions of KIP1, amplifications of CCND2, and structural rearrangements of TEL.

scholarly journals Molecular characterization of 12p abnormalities in hematologic malignancies: deletion of KIP1, rearrangement of TEL, and amplification of CCND2

Blood ◽  
1996 ◽  
Vol 87 (1) ◽  
pp. 324-330 ◽  
Author(s):  
M Hoglund ◽  
B Johansson ◽  
J Pedersen-Bjergaard ◽  
P Marynen ◽  
F Mitelman
Keyword(s):  
Cell Cycle ◽  
In Situ Hybridization ◽  
Tumor Suppressor ◽  
Fluorescence In Situ Hybridization ◽  
Hematologic Malignancies ◽  
Suppressor Gene ◽  
Detectable Change ◽  
Structural Rearrangements

Abstract Twenty patients with hematologic malignancies with 12p abnormalities were investigated by fluorescence in situ hybridization (FISH) using probes mapped to specific regions in 12p. The initial analysis using the YAC 964c10 (D12S736) revealed that all four cases with cytogenetically identified del(12p) had lost one copy of this YAC and that submicroscopic deletions had occurred in 10 of the 16 neoplasms with other 12p abnormalities, ie, translocations, additions, and insertions. The deletions were partially mapped with cosmids localized to subregions of 12p. One copy of the gene for p27kip1 (KIP1), involved in cell cycle entrance, was found to be lost in all cases in which deletions could be detected by other probes and in one case with a translocation as the only detectable change. This implicates KIP1 as a possible tumor suppressor gene affected by del(12p). Four translocations with no apparent concomitant deletions were detected. All four breakpoints resulted in a split D12S736 signal. In two of these cases, we showed that TEL was disrupted as a result of a t(5;12)(q32–33;p12) and a t(12;22)(p12;q12), respectively. Two lymphoid neoplasm--one non-Hodgkin's lymphoma and one Burkitt's lymphoma--with 12p amplifications were detected. In both cases cyclin D2 (CCND2) was within the amplified region. Thus, cytogenetic abnormalities of 12p in hematologic malignancies result in at least three different molecular changes: deletions of KIP1, amplifications of CCND2, and structural rearrangements of TEL.

scholarly journals Centromere position in budding yeast: evidence for anaphase A.

1997 ◽  
Vol 8 (6) ◽  
pp. 957-972 ◽  
Author(s):  
V Guacci ◽  
E Hogan ◽  
D Koshland
Keyword(s):  
Cell Cycle ◽  
In Situ Hybridization ◽  
Fluorescence In Situ Hybridization ◽  
Budding Yeast ◽  
Spindle Pole ◽  
Eukaryotic Cells ◽  
Chromosome Movement ◽  
Yeast Saccharomyces Cerevisiae ◽  
Centromere Position

Although general features of chromosome movement during the cell cycle are conserved among all eukaryotic cells, particular aspects vary between organisms. Understanding the basis for these variations should provide significant insight into the mechanism of chromosome movement. In this context, establishing the types of chromosome movement in the budding yeast Saccharomyces cerevisiae is important since the complexes that mediate chromosome movement (microtubule organizing centers, spindles, and kinetochores) appear much simpler in this organism than in many other eukaryotic cells. We have used fluorescence in situ hybridization to begin an analysis of chromosome movement in budding yeast. Our results demonstrate that the position of yeast centromeres changes as a function of the cell cycle in a manner similar to other eukaryotes. Centromeres are skewed to the side of the nucleus containing the spindle pole in G1; away from the poles in mid-M and clustered near the poles in anaphase and telophase. The change in position of the centromeres relative to the spindle poles supports the existence of anaphase A in budding yeast. In addition, an anaphase A-like activity independent of anaphase B was demonstrated by following the change in centromere position in telophase-arrested cells upon depolymerization and subsequent repolymerization of microtubules. The roles of anaphase A activity and G1 centromere positioning in the segregation of budding yeast chromosomes are discussed. The fluorescence in situ hybridization methodology and experimental strategies described in this study provide powerful new tools to analyze mutants defective in specific kinesin-like molecules, spindle components, and centromere factors, thereby elucidating the mechanism of chromosome movement.

Sign in / Sign up

Export Citation Format

Share Document