The Drosophila ribosomal protein L14-encoding gene, identified by a novel Minute mutation in a dense cluster of previously undescribed genes in cytogenetic region 66D

Sæbøe-Larssen, Stein; Mohebi, Beata U.; Lambertsson, Andrew

doi:10.1007/s004380050482

Cited by 30 publications

(23 citation statements)

References 59 publications

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“…A BLAST search identified a non-66Da gene (Saeboe-Larssen et al 1997) as a possible Drosophila counterpart of human NELF-E. The entire open reading frame encoding a 280-aminoacid protein was amplified using primers 5Ј-CGCATATGGTT TACATACACTTCCCCAAC-3Ј and 5Ј-CGGGATCCTTAGA GCAAGAAGTCTTCATCGTA-3Ј, and a Drosophila embryo cDNA library (Novagen) as template.…”

Section: Cloning and Production Of Antibodiesmentioning

confidence: 99%

NELF and DSIF cause promoter proximal pausing on thehsp70promoter inDrosophila

et al. 2003

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NELF and DSIF collaborate to inhibit elongation by RNA polymerase IIa in extracts from human cells. A multifaceted approach was taken to investigate the potential role of these factors in promoter proximal pausing on the hsp70 gene in Drosophila. Immunodepletion of DSIF from a Drosophila nuclear extract reduced the level of polymerase that paused in the promoter proximal region of hsp70. Depletion of one NELF subunit in salivary glands using RNA interference also reduced the level of paused polymerase. In vivo protein-DNA cross-linking showed that NELF and DSIF associate with the promoter region before heat shock. Immunofluorescence analysis of polytene chromosomes corroborated the cross-linking result and showed that NELF, DSIF, and RNA polymerase IIa colocalize at the hsp70 genes, small heat shock genes, and many other chromosomal locations. Finally, following heat shock induction, DSIF and polymerase but not NELF were strongly recruited to chromosomal puffs harboring the hsp70 genes. We propose that NELF and DSIF cause polymerase to pause in the promoter proximal region of hsp70. The transcriptional activator, HSF, might cause NELF to dissociate from the elongation complex. DSIF continues to associate with the elongation complex and could serve a positive role in elongation.

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Section: Cloning and Production Of Antibodiesmentioning

confidence: 99%

NELF and DSIF cause promoter proximal pausing on thehsp70promoter inDrosophila

et al. 2003

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“…The distribution of Minute loci throughout the genome and the uniformity of the phenotype have been of great interest to geneticists for nearly a century. Many Minute loci correspond to cytoplasmic ribosomal genes, suggesting that the basis of the Minute phenotypes involves disruption of ribosomal function (Hart et al 1993;Andersson et al 1994;Mckim et al 1996;Saeboe-Larssen and Lambertsson 1996;Schmidt et al 1996;Saeboe-Larssen et al 1997;Van Beest et al 1998;Torok et al 1999;Fauvarque et al 2001;Marygold et al 2005;Alexander et al 2006;Tyler et al 2007).…”

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confidence: 99%

Cardiomyopathy Is Associated with Ribosomal Protein Gene Haplo-Insufficiency inDrosophila melanogaster

Casad¹,

Abraham²,

Kim³

et al. 2011

Genetics

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The Minute syndrome in Drosophila melanogaster is characterized by delayed development, poor fertility, and short slender bristles. Many Minute loci correspond to disruptions of genes for cytoplasmic ribosomal proteins, and therefore the phenotype has been attributed to alterations in translational processes. Although protein translation is crucial for all cells in an organism, it is unclear why Minute mutations cause effects in specific tissues. To determine whether the heart is sensitive to haplo-insufficiency of genes encoding ribosomal proteins, we measured heart function of Minute mutants using optical coherence tomography. We found that cardiomyopathy is associated with the Minute syndrome caused by haplo-insufficiency of genes encoding cytoplasmic ribosomal proteins. While mutations of genes encoding non-Minute cytoplasmic ribosomal proteins are homozygous lethal, heterozygous deficiencies spanning these non-Minute genes did not cause a change in cardiac function. Deficiencies of genes for non-Minute mitochondrial ribosomal proteins also did not show abnormal cardiac function, with the exception of a heterozygous disruption of mRpS33. We demonstrate that cardiomyopathy is a common trait of the Minute syndrome caused by haplo-insufficiency of genes encoding cytoplasmic ribosomal proteins. In contrast, most cases of heterozygous deficiencies of genes encoding non-Minute ribosomal proteins have normal heart function in adult Drosophila.

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“…A great challenge for Drosophila geneticists is therefore to understand the functions of the newly discovered genes. anon-66Da (CG5994; GadFly; http://flybase.bio.indiana.edu/annot/), located on chromosome arm 3L at cytological position 66D8 (Saebøe-Larssen et al, 1997), is one of these anonymous genes. The predicted polypeptide of the anon-66Da gene shows homology to the mammalian RD protein, an RNA-binding protein with unknown function (LeviStrauss et al, 1988;Yamaguchi et al, 1999Yamaguchi et al, , 2002.…”

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confidence: 99%

“…Nelf-E was cloned in a P-element mutagenesis experiment, where P{lacW} inserted between the tightly linked Nelf-E and RpL14 genes (Saebøe-Larssen et al, 1997). Attempts to induce mutations in anon-66Da by P-element excision mutagenesis have failed (A. Lambertsson, unpublished results), and we therefore decided to use heritable RNA interference (RNAi) (Kennerdell and Carthew, 2000;Hammond et al, 2001;Adams and Sekelsky, 2002) to generate a mutant phenotype(s) of Nelf-E.…”

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confidence: 99%