Amplification of the X-linked Drosophila chorion gene cluster requires a region upstream from the s38 chorion gene.

Spradling, Allan C.; Cicco, Diane V. de; Wakimoto, Barbara T.; Levine, Jay F.; Kalfayan, L J; Cooley, Lynn

doi:10.1002/j.1460-2075.1987.tb04857.x

Cited by 69 publications

(32 citation statements)

References 55 publications

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“…The origin(s) used during normal chromosomal amplification could be situated anywhere within the 12-to 13-kb central regions of the two major chorion sites and not necessarily at the ACE region (28). Each of the ACEs, however, contains several AATAC repetitive sequence elements and is closely linked to a transcriptional control element, characteristics suggestive of replication origins in that they are similar to several eucaryotic viral origins (10,21,22,28,41). The chromosome III locus contains ars-like repeats as well as two repeats of a 17-mer and several other repeats, extending over the central gene region (9).…”

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confidence: 99%

Visualization of Drosophila melanogaster chorion genes undergoing amplification.

Osheim¹,

Miller²,

Beyer³

1988

Mol. Cell. Biol.

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We visualized by electron microscopy the preferential amplification of Drosophila chorion genes in late-stage follicle cells. Chromatin spreads revealed large clusters of actively transcribed genes of the appropriate size, spacing, and orientation for chorion genes that were expressed with the correct temporal specificity. Occasionally the active genes were observed within or contiguous with intact replicons and replication forks. In every case, our micrographs are consistent with the hypothesis that the central region of each chorion domain contains a replication origin(s) used during the amplification event. In one case, a small replication bubble was observed precisely at the site of the essential region of the X chromosome amplification control element. The micrographs also suggest that forks at either end of a replicon frequently progress very different distances, presumably due to different times in initiation or different rates of movement. It appears that all chorion genes (even those coding for minor proteins) are transcribed in a "fully on" condition, albeit for varied durations, and that if replication fork passage does inactivate a promoter, it does so very transiently. Furthermore, a DNA segment containing one active gene is likely to have an additional active gene (s). Surprisingly, during the time frame of expected maximum activity, approximately half of the chorion sequences appear transcriptionally inactive.The chorion or eggshell in Drosophila mnelanogaster is a complex, proteinaceous structure synthesized during the final 5 h of oogenesis (stages 11 through 14) by follicle cells surrounding the egg chamber (reviewed in reference 23). To accommodate such a high level of protein synthesis from single-copy genes, each of which is expressed for a discrete period, the chorion genes are preferentially amplified in the follicle cells (44). The X-chromosomal locus is amplified 16-to 20-fold, whereas the chromosome III locus undergoes two additional rounds of replication to reach a final amplified level of 64-fold. Amplification is also temporally controlled, occurring during the final 20 h of oogenesis (stages 8 through 13) (19, 27, 40).The major chorion genes which undergo amplification are needed sequentially-s36 and s38 on the X chromosome are transcribed, and their messages are translated primarily during stages 11 and 12 while amplification is still occurring (34). The four short, closely linked genes on the third chromosome (s15, s16, s18, and s19) are utilized during stages 13 and 14, at which time the final round of amplification is being completed (13).Amplification is thought to occur via a mechanism in which multiple initiation events occur in the center of a domain followed by bidirectional fork movement. The forks associated with each successive initiation cover less distance, resulting in a gradient of amplification which decreases smoothly for 40 to 50 kilobases (kb) on both sides of the origin (40). A short region within each of the amplified domains is termed the amplification control...

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mentioning

confidence: 99%

Visualization of Drosophila melanogaster chorion genes undergoing amplification.

Osheim¹,

Miller²,

Beyer³

1988

Mol. Cell. Biol.

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“…1B) by Saito and Stark (32), who cloned a highly amplified joint near the selected CAD gene which brought two copies of this gene close together through an inverted duplication. Ream (10,38) and for rDNA replication in Tetrahymena spp. (21) and has been suggested for the abnormal amplification of a human T-cell differentiation antigen (20).…”

Section: Discussionmentioning

confidence: 99%

Preferential amplification of rearranged sequences near amplified adenylate deaminase genes.

Debatisse¹,

Saito²,

Buttin³

et al. 1988

Mol. Cell. Biol.

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In a previous study of three independent families of mutants selected for overproduction of adenylate deaminase (AMPD), we were not able to isolate a cDNA probe for the gene and so could not demonstrate its amplification directly. In addition to overproduction of AMPD, four proteins of unknown function, designated W, X, Y1, and Y2, accumulated, and by using the corresponding cDNA probes, we demonstrated amplification of anl four genes. In independent mutant clones, sometimes all and sometimes only a subset of these genes were amplified. Assuming that all five genes are linked, the pattern of their coamplification suggested a genetic map in which AMPD lies between W and Y1. We show here that a two-step chromosome walk joins the W and Y1 genes, that the AMPD gene is the only expressed sequence between them, and that its amplification is indeed responsible for overproduction of the AMPD protein. In the course of this work, we cloned and studied two novel joints which mark rearrangements on either side of the AMPD gene. Each joint was generated independently in a single first-step mutant at single or low copy number. Remarkably, each joint was amplified preferentially in every second-and third-step mutant derived from the first-step line in which it was originally present, suggesting that the two independent rearrangements each generated amplification-prone structures.In a number of systems, drug resistance is mediated by gene amplification, and in all cases studied, a sequence much larger than the selected gene is amplified. The first estimates of the average sizes of amplified units-defined as extra DNA sequences containing one copy of the selected geneindicate that they range from about 200 to 3,000 kilobases (kb) in highly resistant cells which have experienced several independent amplification events (for reviews, see references 18, 35, and 39). More recently, a study of the structures formed in the first step of amplification of the CAD gene in Syrian hamster cells has led to the hypothesis that, in this case, the average size of the amplified unit may be 10,000 kb or more (15).Several different techniques have been used to study the structure of the coamplified DNA: cloning of amplified sequences by differential screening (2,4,15) or from purified double minutes (5,14) or homogeneously staining regions (19,43), chromosome walking from the cloned selected genes (11,22), direct visualization of ethidium bromidestained amplified restriction fragments in agarose gels (24,40) and in gel renaturation (12, 31). In most cases, the results point to remarkable differences between the sequences coamplified in independent highly amplified mutants: the amplified units include a region comprising the selected gene and sequences immediately surrounding it in the wild-type line, but also include sequences which are amplified uniquely in each cell line (2,5,12, 34,36,43). Thus, during the amplification process, pieces of DNA from different parts of the genome are joined by recombination to form novel structures and novel join...

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“…It has been established that amplification of a gene cluster in D. melanogaster is controlled by a cis-acting element upstream of the gene (De Cicco and Sprading, 1984;Spradling et al, 1987). Similarly, the existence of a cis-enhancer responsible for the increase in the gene copy number in tobacco (N. tabacum) has been confirmed by genetic transformation (Borisjuk et al, 2000).…”

Section: Molecular Processes Relevant To Dna Content Variationmentioning

confidence: 94%

Developmental and environmental variation in genomes

2009

Heredity

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The genetic make-up of an organism, established at fertilization, is not conventionally expected to change during development unless mutation occurs. However, there is actually evidence that considerable variation can arise. Some of these changes may occur in response to the environment. This article reviews such variations in genome size or DNA content (excluding ploidy-level changes). The variation can be generated by processes, including high-frequency chromosomal recombination, transposition, cis-element-enhanced gene amplification and repetitivesequence-based changes in nuclear DNA content. Environmentally induced and developmentally regulated genomic variation (ED-genomic variation or ED-genetic variation) can be found in both coding and non-coding sequences, and is often non-Mendelian in its inheritance pattern. Changes can depend on development (for example, propagation method, seed/fruit position on plants, embryo stage, etc.) and occur in response to the environment (for example, light, temperature, herbicide, salinity, fertilizer, land slope direction, pathogen infection, etc.). Some plants have meiotic (or rejuvenation) corrections, which restore their genome sizes to a certain degree. However, Mendelian inheritance and acquired inheritance of the variants occur, and both inheritance types may be different expressions evolved for the same adaptive responses. With this perspective, the terms 'pure-breeding line' or 'stable cultivar' may only be appropriate for a given mode of reproduction or propagation, and for a given environment. ED-genomic variation appears to be an essential component of differentiation, development and adaptation. Consequently, modern molecular biology tools, such as microarray hybridization and new sequencing technology, should be directed towards a more comprehensive evaluation of ED-genomic variation.

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Amplification of the X-linked Drosophila chorion gene cluster requires a region upstream from the s38 chorion gene.

Cited by 69 publications

References 55 publications

Visualization of Drosophila melanogaster chorion genes undergoing amplification.

Visualization of Drosophila melanogaster chorion genes undergoing amplification.

Preferential amplification of rearranged sequences near amplified adenylate deaminase genes.

Developmental and environmental variation in genomes

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