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  Elimination of a group II intron from a plastid gene causes a mutant phenotype

Petersen, K., Schöttler, M. A., Karcher, D., Thiele, W., & Bock, R. (2011). Elimination of a group II intron from a plastid gene causes a mutant phenotype. Nucleic Acids Research, 39(12), 5181-5192. doi:10.1093/nar/gkr105.

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 Creators:
Petersen, K.1, Author              
Schöttler, M. A.2, Author              
Karcher, D.1, Author              
Thiele, W.1, Author              
Bock, R.1, Author              
Affiliations:
1Organelle Biology and Biotechnology, Department Bock, Max Planck Institute of Molecular Plant Physiology, Max Planck Society, ou_1753326              
2Photosynthesis Research, Department Bock, Max Planck Institute of Molecular Plant Physiology, Max Planck Society, ou_1753323              

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Free keywords: domain protein functions photosystem-i arabidopsis-thaliana chlamydomonas-reinhardtii maize chloroplasts encoded proteins splicing factors messenger-rna tobacco temperature
 Abstract: Group II introns are found in bacteria and cell organelles (plastids, mitochondria) and are thought to represent the evolutionary ancestors of spliceosomal introns. It is generally believed that group II introns are selfish genetic elements that do not have any function. Here, we have scrutinized this assumption by analyzing two group II introns that interrupt a plastid gene (ycf3) involved in photosystem assembly. Using stable transformation of the plastid genome, we have generated mutant plants that lack either intron 1 or intron 2 or both. Interestingly, the deletion of intron 1 caused a strong mutant phenotype. We show that the mutants are deficient in photosystem I and that this deficiency is directly related to impaired ycf3 function. We further show that, upon deletion of intron 1, the splicing of intron 2 is strongly inhibited. Our data demonstrate that (i) the loss of a group II intron is not necessarily phenotypically neutral and (ii) the splicing of one intron can depend on the presence of another.

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Language(s): eng - English
 Dates: 2011-02-262011
 Publication Status: Published in print
 Pages: -
 Publishing info: -
 Table of Contents: -
 Rev. Type: -
 Identifiers: ISI: ISI:000292564900031
DOI: 10.1093/nar/gkr105
ISSN: 0305-1048
URI: ://000292564900031http://nar.oxfordjournals.org/content/39/12/5181
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Title: Nucleic Acids Research
  Other : Nucleic Acids Res.
Source Genre: Journal
 Creator(s):
Affiliations:
Publ. Info: -
Pages: - Volume / Issue: 39 (12) Sequence Number: - Start / End Page: 5181 - 5192 Identifier: ISSN: 0301-5610
CoNE: https://pure.mpg.de/cone/journals/resource/1000000000262810