Perinuclear Mlp proteins downregulate gene expression in response to a defect in mRNA export

Autor: Nahid Iglesias, Daniel Zenklusen, Patrizia Vinciguerra, Françoise Stutz, Jurgi Camblong
Jazyk: angličtina
Rok vydání: 2005
Předmět:
Saccharomyces cerevisiae Proteins
Mutation/genetics
Transcription
Genetic
RNA
Messenger/genetics/metabolism
Lac Operon/genetics
RNA Stability
Mutant
lac operon
Down-Regulation
RNA-binding protein
Saccharomyces cerevisiae
Biology
Saccharomyces cerevisiae Proteins/genetics/metabolism
General Biochemistry
Genetics and Molecular Biology
Article
RNA Transport
Transcription (biology)
ddc:570
Gene Expression Regulation
Fungal
Gene expression
RNA
Messenger
RNA-Binding Proteins/genetics/metabolism
Molecular Biology
Nuclear Proteins/deficiency/genetics/metabolism
In Situ Hybridization
Transcription
Genetic/genetics
RNA
Fungal/genetics/metabolism
Messenger RNA
General Immunology and Microbiology
General Neuroscience
Ribonucleoproteins/metabolism
Temperature
RNA
Nuclear Proteins
RNA-Binding Proteins
RNA
Fungal
Beta-Galactosidase/genetics/metabolism
Down-Regulation/genetics
beta-Galactosidase
Molecular biology
Nuclear Pore Complex Proteins
Phenotype
Lac Operon
Ribonucleoproteins
Mutation
Chromatin immunoprecipitation
Saccharomyces cerevisiae/genetics/metabolism
Gene Deletion
Protein Binding
Zdroj: EMBO Journal, Vol. 24, No 4 (2005) pp. 813-23
ISSN: 0261-4189
Popis: The mRNA export adaptor Yra1p/REF contributes to nascent mRNP assembly and recruitment of the export receptor Mex67p. yra1 mutants exhibit mRNA export defects and a decrease in LacZ reporter and certain endogenous transcripts. The loss of Mlp1p/Mlp2p, two TPR-like proteins attached to nuclear pores, rescues LacZ mRNA levels and increases their appearance in the cytoplasm, without restoring bulk poly(A)+ RNA export. Chromatin immunoprecipitation, FISH and pulse-chase experiments indicate that Mlps downregulate LacZ mRNA synthesis in a yra1 mutant strain. Microarray analyses reveal that Mlp2p also reduces a subset of cellular transcripts in the yra1 mutant. Finally, we show that Yra1p genetically interacts with the shuttling mRNA-binding protein Nab2p and that loss of Mlps rescues the growth defect of yra1 and nab2 but not other mRNA export mutants. We propose that Nab2p and Yra1p are required for proper mRNP docking to the Mlp platform. Defects in Yra1p prevent mRNPs from crossing the Mlp gate and this block negatively feeds back on the transcription of a subset of genes, suggesting that Mlps link mRNA transcription and export.
Databáze: OpenAIRE
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