ArticleMolecular and cellular biology1994
The SR protein B52/SRp55 is essential for Drosophila development.
Article in Molecular and cellular biology, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
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Who cites it
64 citing papers in PubMed.
- Alternative splicing perspective to prey preference of environmentally friendly biological agent Cryptolaemus montrouzieri.BMC genomics · 2024Article
- Regulation of theRNA (New York, N.Y.) · 2024Article
- SRSF6 balances mitochondrial-driven innate immune outcomes through alternative splicing of BAX.eLife · 2022Article
- SRSF6 Regulates the Alternative Splicing of the Apoptotic Fas Gene by Targeting a Novel RNA Sequence.Cancers · 2022Article
- Targeting Splicing Factor SRSF6 for Cancer Therapy.Frontiers in cell and developmental biology · 2021Review
- The SR protein B52/SRp55 regulates splicing of the period thermosensitive intron and mid-day siesta in Drosophila.Scientific reports · 2018Article
- Number of inadvertent RNA targets for morpholino knockdown in Danio rerio is largely underestimated: evidence from the study of Ser/Arg-rich splicing factors.Nucleic acids research · 2017Article
- Protein sequestration as a normal function of long noncoding RNAs and a pathogenic mechanism of RNAs containing nucleotide repeat expansions.Human genetics · 2017Review
- Controlling the Master: Chromatin Dynamics at the MYC Promoter Integrate Developmental Signaling.Genes · 2017Review
- Single neuron transcriptomics identify SRSF/SR protein B52 as a regulator of axon growth and Choline acetyltransferase splicing.Scientific reports · 2016Article
- Regulation of splicing factors by alternative splicing and NMD is conserved between kingdoms yet evolutionarily flexible.Molecular biology and evolution · 2015Article
- A role for the serine/arginine-rich (SR) protein B52/SRSF6 in cell growth and myc expression in Drosophila.Genetics · 2015Article
- The SR protein B52/SRp55 is required for DNA topoisomerase I recruitment to chromatin, mRNA release and transcription shutdown.PLoS genetics · 2010Article
- Identification of small molecule and genetic modulators of AON-induced dystrophin exon skipping by high-throughput screening.PloS one · 2009Article
- Specific combinations of SR proteins associate with single pre-messenger RNAs in vivo and contribute different functions.The Journal of cell biology · 2009Article
- Identification of RNA binding sequences of Drosophila SR protein DX16.Molecular and cellular biochemistry · 2007Article
- The impact of alternative splicing in vivo: mouse models show the way.RNA (New York, N.Y.) · 2007Review
- TASR-1 regulates alternative splicing of collagen genes in chondrogenic cells.Biochemical and biophysical research communications · 2007Article
- The SR family proteins B52 and dASF/SF2 modulate development of the Drosophila visual system by regulating specific RNA targets.Molecular and cellular biology · 2007Article
- Eye development under the control of SRp55/B52-mediated alternative splicing of eyeless.PloS one · 2007Article
4 more citing papers are in PubMed but not listed here.
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2 authors.
Funding
Abstract
B52, also called SRp55, is a 52-kDa member of the Drosophila SR protein family of general splicing factors. Escherichia coli-produced B52 is capable of both activating splicing and affecting the alternative splice site choice in human in vitro splicing reactions. Here we report the isolation of a B52 null mutant generated by remobilizing a P element residing near the B52 gene. The resulting deletion, B52(28), is confined to the B52 gene and its neighbor the Hrb87F gene. Second-instar larvae homozygous for the deletion are deficient in both B52 mRNA and protein. The B52 null mutant is lethal at the first- and second-instar larval stages. Germ line transformation of Drosophila flies with B52 genomic DNA rescues this lethality. Thus, B52 is an essential gene and has a critical role in Drosophila development. Larvae deficient in B52 are still capable of splicing the five endogenous pre-mRNAs tested here, including both constitutively and alternatively spliced genes. Therefore, B52 is not required for all splicing in vivo. This is the first in vivo deficiency analysis of a member of the SR protein family.
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