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Array CGH of Drosophila compound chromosomes on heterochromatin custom array.

ABSTRACT: Mapping the Drosophila melanogaster centromeric heterochromatin by CGH analysis of embryos lacking specific chromosomes or chromosome arms.

ORGANISM(S): Drosophila melanogaster

PROVIDER: GSE36260 | GEO | 2012/03/06

SECONDARY ACCESSION(S): PRJNA153083

REPOSITORIES: GEO

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Array CGH of Drosophila compound chromosomes on heterochromatin custom array.

Project description:Mapping the Drosophila melanogaster centromeric heterochromatin by CGH analysis of embryos lacking specific chromosomes or chromosome arms. Nine chromosome or chromosome arm deletions were tested: embryos lacking the entire second chromosome (2En-), 2L (2L-), 2R (2R-), the entire third chromosome (3En-), 3L (3L-), 3R (3R-), the entire fourth chromosome (4En-), the X chromosome (X-), or both X and Y chromosomes (XY-). Control: Blastoderm stage wild type Oregon R embryos. For each experiment 100-150 embryos of the appropriate genotype were collected. DNA from randomly staged 0-8 hr wild type Oregon R embryos was used as reference for all experiments. Embryos with no X chromosome were obtained by crossing attached-X/Y females (C(1)DX, y f) to X/Y males. Embryos with no X and Y chromosomes were obtained by crossing attached-X/Y females (C(1)RM, y2suwawa) to attached-XY males (YSX YL, In(1)EN, y B). The compound II chromosomes RM(2L); RM(2R)=C(2)v and the compound III chromosomes RM(3L); RM(3R)=C(3)se were used to generate 2L- and 2R-, and 3L- and 3R- embryos, respectively. The compound II C(2)EN and compound III C(3)EN st1 cu1es stocks were used to generate embryos deficient for the entire second and third chromosome, respectively. The compound IV C(4)RM, ci1eyR/0 were used to generate embryos deficient for the fourth chromosome. Embryos deficient for chromosome 4 were identified by their defects in denticle belt patterning during late embryogenesis, whereas embryos deficient for other chromosome/chromosome arm were recognized based on their specific phenotypic defects during early embryonic development. All embryos were collected at room temperature.

2012-03-06 | E-GEOD-36260 | biostudies-arrayexpress

Array CGH of Drosophila translocations on heterochromatin custom array-eu_het boundary.

Project description:CGH analysis of translocations with breakpoints at the euchromatin/heterochromatin boundary. Three translocations with breakpoint at the euchromatin/heterochromatin boundary of 2L, 3L and X, respectively, were analyzed by CGH to distinguish heterochromatic sequences from euchromatic sequences. X: 101042(T(1;Y)B91); 2L: 130186 (T(Y;2)R146); and 3L: 102004(T(2;3)H31). To obtain embryos lacking the euchromatin portion of the chromosome arms, translocation males bearing breakpoint at the euchromatin/heterochromatin boundary of 2L, 3L and X were crossed to C(2)EN, C(3)EN or attached X females, respectively. All embryos were collected at room temperature.

2012-03-06 | E-GEOD-36261 | biostudies-arrayexpress

Array CGH of Drosophila polytene chromosomes on heterochromatin custom array.

Project description:CGH analysis of Drosophila polytene chromosomes.

2012-03-06 | GSE36264 | GEO

Array CGH of Drosophila translocations on heterochromatin custom array-2Rhet.

Project description:Mapping the Drosophila melanogaster 2R heterochromatin by CGH analysis of embryos lacking specific regions of 2R.

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Array CGH of Drosophila ChrX deficiencies_duplications on heterochromatin custom array.

Project description:Mapping the Drosophila melanogaster X heterochromatin by CGH analysis of embryos lacking specific regions of the X chromosome.

2012-03-06 | GSE36262 | GEO

Array CGH of Drosophila translocations on heterochromatin custom array-eu_het boundary.

Project description:CGH analysis of translocations with breakpoints at the euchromatin/heterochromatin boundary.

2012-03-06 | GSE36261 | GEO

Array CGH of Drosophila polytene chromosomes on heterochromatin custom array.

Project description:CGH analysis of Drosophila polytene chromosomes. Drosophila polytene chromosomes were isolated from whole salivary glands dissected from roaming third-instar larvae or from ovaries dissected from adult females. Salivary gland has two biological repeats.

2012-03-06 | E-GEOD-36264 | biostudies-arrayexpress

Array CGH of Drosophila translocations on heterochromatin custom array-2Rhet.

Project description:Mapping the Drosophila melanogaster 2R heterochromatin by CGH analysis of embryos lacking specific regions of 2R. Seven translocations with breakpoints in 2R heterochromatin were tested: 2219 (T(2;3)ftz[Rpl]), 130058 (T(Y;2)B[SV5]), 130093 (T(Y;2)B63), 130112 (T(Y;2)B238), 101579 (T(2;3)bxd[68]), 101988 (T(Y;2)G10), and 107387 (T(2;3)E(da)). To generate embryos deficient for smaller regions of 2R heterochromatin, T(2;Y) or T(2;3) translocation males were crossed to C(2)EN females. One eighth of the embryos that lack 2R were identified according to their failure in forming the ventral furrow during early gastrulation. All embryos were collected at room temperature.

2012-03-06 | E-GEOD-36263 | biostudies-arrayexpress

Array CGH of Drosophila ChrX deficiencies_duplications on heterochromatin custom array.

Project description:Mapping the Drosophila melanogaster X heterochromatin by CGH analysis of embryos lacking specific regions of the X chromosome. Eight ChrX deficiencies and duplications were tested: 168 (Dp(1;Y)y[2]67g), 175 (Dp(1;Y)y[2]sc), 114n (Dp(1;Y)y[+]mal[126]), 114f (Df(1)fog[114]), 186n (Dp(1;Y)y[+]mal), 186f (Df(1)mal12), B2580 (Dp(1;Y)ct y[+]), B5280 (Dp(1;Y)ct[+]y[+]). To generate embryos lacking different portions of the X heterochromatin, two types of stocks were used: (1) males carrying a deficient X chromosome missing part of the heterochromatin (generally fog-) and a duplication on the Y chromosome that complements the deficiency, and (2) males carrying a duplication of X on the Y chromosome which covers part of the X heterochromatin. In both cases males were crossed to attached X females. In the first case, one quarter of embryos lack most of the X chromosome except the duplication of X on Y. These embryos were identified according to their defects during cellularization. Another quarter of the embryos carry the deficient X chromosome as their sole X chromosome. These embryos were identified according to their defects in posterior midgut formation during early gastrulation. In the second case, one quarter of embryos that lack most of the X chromosome except the duplication of X on Y were identified according to their defects in cellularization or posterior midgut formation. All embryos were collected at room temperature.

2012-03-06 | E-GEOD-36262 | biostudies-arrayexpress

Heterochromatin protein 1 (HP1) modulates replication timing of Drosophila heterochromatin

Project description:The replication of a genomic region during S-phase can be highly dynamic between cell types that differ in transcriptome and epigenome. Replication timing has been positively correlated with several histone modifications that occur at active genes, while repressive histone modifications mark late replicating regions. This raises the question if chromatin modulates the initiating events of replication. To gain insights into this question we have studied the function of heterochromatin protein 1 (HP1), a reader of to the repressive histone lysine 9 methylation of H3, in genome-wide organization of replication. Cells with reduced levels of HP1 show an advanced replication timing of centromeric repeats in agreement with the model that repressive chromatin mediates the very late replication of large clusters of constitutive heterochromatin. Surprisingly however regions with high levels of interspersed repeats on the chromosomal arms in particular on chromosome 4 and in pericentromeric regions of chromosome 2 behave differently. Here loss of HP1 results in delayed replication timing. The fact that these regions are bound by HP1 suggests a direct effect. Thus while HP1 mediates very late replication of centromeric DNA it is also required for early replication of autosomal regions with high levels of repeats. This observation of opposing functions of HP1 suggests a model where repeat inactivation on autosomes is required for proper activation of origins of replication that fire early, while HP1 mediated repression at constitutive heterochromatin is required to ensure replication of centromeric repeats at the end of S phase. Keywords: RNAi, chip-chip, replication timing

2010-03-16 | GSE18092 | GEO

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