2013
Akay, Alper; Craig, Ashley; Lehrbach, Nicolas; Larance, Mark; Pourkarimi, Ehsan; Wright, Jane E; Lamond, Angus; Miska, Eric; Gartner, Anton
RNA-binding protein GLD-1/quaking genetically interacts with the mir-35 and the let-7 miRNA pathways in Caenorhabditis elegans Journal Article
In: Open Biol., vol. 3, no. 11, pp. 130151, 2013, ISSN: 2046-2441.
Abstract | Links | BibTeX | Tags: Caenorhabditis elegans, gld-1, let-7, miRNA, SILAC
@article{akay_rna-binding_2013,
title = {RNA-binding protein GLD-1/quaking genetically interacts with the mir-35 and the let-7 miRNA pathways in Caenorhabditis elegans},
author = {Alper Akay and Ashley Craig and Nicolas Lehrbach and Mark Larance and Ehsan Pourkarimi and Jane E Wright and Angus Lamond and Eric Miska and Anton Gartner},
url = {http://dx.doi.org/10.1098/rsob.130151},
doi = {10.1098/rsob.130151},
issn = {2046-2441},
year = {2013},
date = {2013-11-01},
journal = {Open Biol.},
volume = {3},
number = {11},
pages = {130151},
abstract = {Messenger RNA translation is regulated by RNA-binding proteins and small
non-coding RNAs called microRNAs. Even though we know the majority of
RNA-binding proteins and microRNAs that regulate messenger RNA expression,
evidence of interactions between the two remain elusive. The role of the
RNA-binding protein GLD-1 as a translational repressor is well studied
during Caenorhabditis elegans germline development and maintenance.
Possible functions of GLD-1 during somatic development and the mechanism
of how GLD-1 acts as a translational repressor are not known. Its human
homologue, quaking (QKI), is essential for embryonic development. Here, we
report that the RNA-binding protein GLD-1 in C. elegans affects multiple
microRNA pathways and interacts with proteins required for microRNA
function. Using genome-wide RNAi screening, we found that nhl-2 and vig-1,
two known modulators of miRNA function, genetically interact with GLD-1.
gld-1 mutations enhance multiple phenotypes conferred by mir-35 and let-7
family mutants during somatic development. We used stable isotope
labelling with amino acids in cell culture to globally analyse the changes
in the proteome conferred by let-7 and gld-1 during animal development. We
identified the histone mRNA-binding protein CDL-1 to be, in part,
responsible for the phenotypes observed in let-7 and gld-1 mutants. The
link between GLD-1 and miRNA-mediated gene regulation is further supported
by its biochemical interaction with ALG-1, CGH-1 and PAB-1, proteins
implicated in miRNA regulation. Overall, we have uncovered genetic and
biochemical interactions between GLD-1 and miRNA pathways.},
keywords = {Caenorhabditis elegans, gld-1, let-7, miRNA, SILAC},
pubstate = {published},
tppubtype = {article}
}
Messenger RNA translation is regulated by RNA-binding proteins and small
non-coding RNAs called microRNAs. Even though we know the majority of
RNA-binding proteins and microRNAs that regulate messenger RNA expression,
evidence of interactions between the two remain elusive. The role of the
RNA-binding protein GLD-1 as a translational repressor is well studied
during Caenorhabditis elegans germline development and maintenance.
Possible functions of GLD-1 during somatic development and the mechanism
of how GLD-1 acts as a translational repressor are not known. Its human
homologue, quaking (QKI), is essential for embryonic development. Here, we
report that the RNA-binding protein GLD-1 in C. elegans affects multiple
microRNA pathways and interacts with proteins required for microRNA
function. Using genome-wide RNAi screening, we found that nhl-2 and vig-1,
two known modulators of miRNA function, genetically interact with GLD-1.
gld-1 mutations enhance multiple phenotypes conferred by mir-35 and let-7
family mutants during somatic development. We used stable isotope
labelling with amino acids in cell culture to globally analyse the changes
in the proteome conferred by let-7 and gld-1 during animal development. We
identified the histone mRNA-binding protein CDL-1 to be, in part,
responsible for the phenotypes observed in let-7 and gld-1 mutants. The
link between GLD-1 and miRNA-mediated gene regulation is further supported
by its biochemical interaction with ALG-1, CGH-1 and PAB-1, proteins
implicated in miRNA regulation. Overall, we have uncovered genetic and
biochemical interactions between GLD-1 and miRNA pathways.
non-coding RNAs called microRNAs. Even though we know the majority of
RNA-binding proteins and microRNAs that regulate messenger RNA expression,
evidence of interactions between the two remain elusive. The role of the
RNA-binding protein GLD-1 as a translational repressor is well studied
during Caenorhabditis elegans germline development and maintenance.
Possible functions of GLD-1 during somatic development and the mechanism
of how GLD-1 acts as a translational repressor are not known. Its human
homologue, quaking (QKI), is essential for embryonic development. Here, we
report that the RNA-binding protein GLD-1 in C. elegans affects multiple
microRNA pathways and interacts with proteins required for microRNA
function. Using genome-wide RNAi screening, we found that nhl-2 and vig-1,
two known modulators of miRNA function, genetically interact with GLD-1.
gld-1 mutations enhance multiple phenotypes conferred by mir-35 and let-7
family mutants during somatic development. We used stable isotope
labelling with amino acids in cell culture to globally analyse the changes
in the proteome conferred by let-7 and gld-1 during animal development. We
identified the histone mRNA-binding protein CDL-1 to be, in part,
responsible for the phenotypes observed in let-7 and gld-1 mutants. The
link between GLD-1 and miRNA-mediated gene regulation is further supported
by its biochemical interaction with ALG-1, CGH-1 and PAB-1, proteins
implicated in miRNA regulation. Overall, we have uncovered genetic and
biochemical interactions between GLD-1 and miRNA pathways.