Change search
ReferencesLink to record
Permanent link

Direct link
The YrdC protein - a putative ribosome maturation factor
Stockholm University, Faculty of Science, Department of Genetics, Microbiology and Toxicology.
2005 (English)In: Biochimica et Biophysica Acta, Gene Structure and Expression, ISSN 0167-4781, E-ISSN 1879-2634, Vol. 1727, no 2, 87-96 p.Article in journal (Refereed) Published
Abstract [en]

Release factor one (RF1) terminates protein synthesis in response to stop codons UAG and UAA. A mutant allele of RF1 causes temperature sensitive growth at 42 °C. We have earlier described the isolation of a suppressor of the temperature sensitive phenotype. The suppressor mutation is a small deletion in the open reading frame yrdC, and we have shown that the ΔyrdC mutation leads to immature 30S subunits and, as a consequence, to fewer translating ribosomes. YrdC is a small conserved protein with a dsRNA-binding surface. Here, we have characterized the YrdC protein. We show that the deletion leads to no production of functional protein, and we have indications that the YrdC protein might be essential in a wild type background. The protein is needed for the maturation of 16S rRNA, even though it does not interact tightly with either of the ribosomal subunits, or the 70S particles. The less effective maturation of rRNA affects the ribosomal feedback control, leading to an increase in expression from P1rrnB. We suggest that the function of the YrdC protein is to keep an rRNA structure needed for proper processing of 16S rRNA, especially at lower temperatures. This activity may require other factor(s). We suggest the gene be renamed rimN, and the mutant allele rimN141.

Place, publisher, year, edition, pages
Elsevier B.V , 2005. Vol. 1727, no 2, 87-96 p.
Keyword [en]
Release factor one; 17S rRNA; Ribosome biogenesis; RimN; YciO; SUA5
National Category
Microbiology in the medical area
URN: urn:nbn:se:su:diva-23421DOI: 10.1016/j.bbaexp.2004.11.010OAI: diva2:191998
Part of urn:nbn:se:su:diva-288Available from: 2004-11-18 Created: 2004-11-18 Last updated: 2010-09-29Bibliographically approved
In thesis
1. Study of the Link between Translation Termination and Ribosome Biogenesis
Open this publication in new window or tab >>Study of the Link between Translation Termination and Ribosome Biogenesis
2004 (English)Doctoral thesis, comprehensive summary (Other academic)
Abstract [en]

Release factor 1 (RF1) is a ribosome-binding protein required for termination of translation in Escherichia coli. To study the effect of slow termination on protein synthesis, two isolated suppressors to a temperature sensitive (Ts) mutant allele of RF1 were studied. The first mutation, rpsIt2215, located within the transcription terminator for the rplM operon, affects expression of ribosomal protein S9. This protein is part of the head domain of the small ribosomal subunit and facilitates mRNA accommodation during translation initiation. The second mutation is a small deletion of the initiation region of gene rimN. rimN141 leads to no production of functional protein, which in wild type is essential for 16S rRNA maturation. Still, even though the RimN protein contains a dsRNA-binding surface, it does not bind tightly to the ribosome. RimN’s probable function in 16S rRNA processing is to resolve and refold intermediate rRNA structures.

Both rpsIt2215 and rimN141 affect maturation of 30S ribosomal subunit. The defect can be observed as a decrease in the amount of translating ribosomes, and as shown in the case of rimN141, also induced expression of rRNA. The affected 30S assembly and translation initiation might be part of the mutant RF1 suppression mechanism, acting through increased cellular RF1 concentrations or a decreased requirement for efficient termination.

Not much is known about how the expression of RF1 is regulated. RF1 is encoded by the prfA gene, located as the second gene in the hemA operon. Three promoters have been suggested to regulate its transcription. Two of them, promoters P1hemA and P2hemA, are located upstream of hemA, the first gene in the operon. P1hemA is the stronger promoter and has been suggested to be regulated upon changes in growth rate and (p)ppGpp concentrations. However, our results do not support this view. The third promoter, PprfA, is putative and the +1 start site of transcription is located to the hemA-coding region.

Place, publisher, year, edition, pages
Stockholm: Institutionen för genetik, mikrobiologi och toxikologi, 2004. 62 p.
National Category
urn:nbn:se:su:diva-288 (URN)91-7265-961-0 (ISBN)
Public defence
2004-12-09, Nordenskiöldsalen, Geovetenskapens hus, Svante Arrhenius väg 8 C, Stockholm, 10:00
Available from: 2004-11-18 Created: 2004-11-18Bibliographically approved

Open Access in DiVA

No full text

Other links

Publisher's full text
By organisation
Department of Genetics, Microbiology and Toxicology
In the same journal
Biochimica et Biophysica Acta, Gene Structure and Expression
Microbiology in the medical area

Search outside of DiVA

GoogleGoogle Scholar
The number of downloads is the sum of all downloads of full texts. It may include eg previous versions that are now no longer available

Altmetric score

Total: 93 hits
ReferencesLink to record
Permanent link

Direct link