The Multi-AT-Hook Chromosomal Protein of <i>Drosophila melanogaster</i>, D1, Is Dispensable for Viability

Weiler, Karen S.; Chatterjee, Suman

doi:10.1534/genetics.109.101386

Cited by 3 publications

(8 citation statements)

References 52 publications

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“…We have previously shown that D1-null flies are viable and fertile and do not exhibit any obvious phenotypic abnormalities (Weiler and Chatterjee 2009). We also determined that although the D1 protein localizes to heterochromatin, D1 mutants are not modifiers of position effect variegation.…”

Section: Discussionmentioning

confidence: 71%

“…Similar to mammalian HMGA proteins (Fusco and Fedele 2007), Drosophila D1 is not essential for viability. D1-null animals were fertile and did not exhibit any obvious phenotypes that would illuminate the cellular role of the D1 protein (Weiler and Chatterjee 2009). This result indicates that there is redundancy to D1 function.…”

Section: Introductionmentioning

confidence: 88%

“…The isolation of the precise excision derivative of the P element insertion P{EP}D1 EP473 , D1 Rev1B , and the D1 deficiency, Df(3R)D1 C12w-, were described in Weiler and Chatterjee (2009). The P{w + , tubP-GAL4}LL7 (stock 5138), P{w + , Act5C-GAL4}25FO1 (stock 4414), P {w + , Act5C-GAL4}17bFO1 (stock 3954), P{w + , GAL4-Hsp70.PB} (stock 5704), P{w + , ey3.5-GAL4.Exel}3 (stock 8219), P{w + , GAL4-ninaE.GMR}12 (stock 1104), P{GawB} sca 109-68 (stock 6479), P{w + , GAL4-nos.NGT}40 (stock 4442), P{w + , GAL4::VP16-nos.UTR}MVD1 (stock 4937), P {w + , matα4GAL4:VP16}V2H (stock 7062), TM3, P{GAL4-twi.G}2.3, P{UAS-2xEGFP}AH2.3, Sb 1 Ser 1 (stock 6663), and P{UAS-GFP-lacZ.nls}15.3 (stock 6451) strains derived from BDSC.…”

Section: Drosophila Strains and Culture Conditionsmentioning

confidence: 99%

“…HMGN proteins are not found in Drosophila, and a strict orthologue of mammalian HMGA is also not present. However, the D1 protein is a multi-AT-hook protein that shares most of the biochemical properties of HMGA proteins, with the exception of its larger size, and we and others consider it to be the Drosophila counterpart of HMGA (Ashley et al 1989;Renner et al 2000;Aleporou-Marinou et al 2003;Weiler and Chatterjee 2009).…”

Section: Introductionmentioning

confidence: 98%

“…We recently isolated D1-null mutations in order to assess the D1 loss-of-function phenotype (Weiler and Chatterjee 2009). Similar to mammalian HMGA proteins (Fusco and Fedele 2007), Drosophila D1 is not essential for viability.…”

Section: Introductionmentioning

confidence: 99%

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Drosophila D1 overexpression induces ectopic pairing of polytene chromosomes and is deleterious to development

Smith

Weiler

2010

Chromosoma

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Eukaryotic genomes function in the context of chromatin, but the roles of most nonhistone chromosomal proteins are far from understood. The D1 protein of Drosophila is an example of a chromosomal protein that has been fairly well characterized biochemically, but has nevertheless eluded functional description. To this end, we have undertaken a gain-of-function genetical analysis of D1, utilizing the GAL4-UAS system. We determined that ubiquitous overexpression of D1 using the Act5C- or tubP-GAL4 drivers was lethal to the organism during larval growth. We also ectopically expressed D1 in a tissue-limited manner using other GAL4 drivers. In general, ectopic D1 was observed to inhibit differentiation and/or development. We observed effects on pattern formation of the adult eye, bristle morphogenesis, and spermatogenesis. These phenotypes may be the consequence of misregulation of D1 target genes. A surprising result was obtained when D1 was overexpressed in the third instar salivary gland. The polytene chromosomes exhibited numerous ectopic associations such that spreading of the chromosome arms was precluded. We mapped the sites of ectopic pairing along the polytene chromosome arms, and found a correlation with sites of intercalary heterochromatin. We speculate that these sites comprise the natural targets of D1 protein activity and that D1 is involved in the ectopic pairing observed for wild-type chromosomes. Together, our data suggest that D1 may influence multiple biochemical activities within the nucleus.

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Section: Discussionmentioning

confidence: 71%

Section: Introductionmentioning

confidence: 88%

Section: Drosophila Strains and Culture Conditionsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 98%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Drosophila D1 overexpression induces ectopic pairing of polytene chromosomes and is deleterious to development

Smith

Weiler

2010

Chromosoma

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Genetic Screen in Drosophila Larvae Links ird1 Function to Toll Signaling in the Fat Body and Hemocyte Motility

Schmid

Ines

et al. 2016

PLoS ONE

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To understand how Toll signaling controls the activation of a cellular immune response in Drosophila blood cells (hemocytes), we carried out a genetic modifier screen, looking for deletions that suppress or enhance the mobilization of sessile hemocytes by the gain-of-function mutation Toll10b (Tl10b). Here we describe the results from chromosome arm 3R, where five regions strongly suppressed this phenotype. We identified the specific genes immune response deficient 1 (ird1), headcase (hdc) and possibly Rab23 as suppressors, and we studied the role of ird1 in more detail. An ird1 null mutant and a mutant that truncates the N-terminal kinase domain of the encoded Ird1 protein affected the Tl10b phenotype, unlike mutations that affect the C-terminal part of the protein. The ird1 null mutant suppressed mobilization of sessile hemocytes, but enhanced other Tl10b hemocyte phenotypes, like the formation of melanotic nodules and the increased number of circulating hemocytes. ird1 mutants also had blood cell phenotypes on their own. They lacked crystal cells and showed aberrant formation of lamellocytes. ird1 mutant plasmatocytes had a reduced ability to spread on an artificial substrate by forming protrusions, which may explain why they did not go into circulation in response to Toll signaling. The effect of the ird1 mutation depended mainly on ird1 expression in hemocytes, but ird1-dependent effects in other tissues may contribute. Specifically, the Toll receptor was translocated from the cell membrane to intracellular vesicles in the fat body of the ird1 mutant, and Toll signaling was activated in that tissue, partially explaining the Tl10b-like phenotype. As ird1 is otherwise known to control vesicular transport, we conclude that the vesicular transport system may be of particular importance during an immune response.

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Analyzing the role of CK2 and PP2A in Drosophila position effect variegation

Banerjee¹

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The results of the investigation into the role of CK2 and PP2A in Drosophila position effect variegation (PEV) and chromatin modification are presented here. PEV is seen when a gene normally found in euchromatin is placed in close proximity to heterochromatin. The propensity of heterochromatin to spread down the chromosome often results in inactivation of the displaced gene by compaction into heterochromatin. The study presented here utilized two different PEV reporter genes for investigating the role of two posttranslational modifying enzymes, the kinase CK2 and the phosphatase PP2A in chromatin formation. The reporter genes used in this study encode for specific eye color and bristle phenotypes or morphology. The expression of these genes is affected when juxtaposed to heterochromatin, thus serving as a strong reporter to monitor the heterochromatic spread in PEV. Studies revealed that CK2 activity is required for either the establishment, maintenance, or perpetuation of euchromatin or, negatively controls the formation of heterochromatin. PP2A, on the other hand, acts in the opposite fashion-either by favoring the formation of heterochromatin or by inhibiting euchromatin.

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The Multi-AT-Hook Chromosomal Protein of Drosophila melanogaster, D1, Is Dispensable for Viability

Cited by 3 publications

References 52 publications

Drosophila D1 overexpression induces ectopic pairing of polytene chromosomes and is deleterious to development

Drosophila D1 overexpression induces ectopic pairing of polytene chromosomes and is deleterious to development

Genetic Screen in Drosophila Larvae Links ird1 Function to Toll Signaling in the Fat Body and Hemocyte Motility

Analyzing the role of CK2 and PP2A in Drosophila position effect variegation

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