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

MPS-Authors
http://pubman.mpdl.mpg.de/cone/persons/resource/persons97337

Petersen,  K.
Organelle Biology and Biotechnology, Department Bock, Max Planck Institute of Molecular Plant Physiology, Max Planck Society;

http://pubman.mpdl.mpg.de/cone/persons/resource/persons97392

Schöttler,  M. A.
Photosynthesis Research, Department Bock, Max Planck Institute of Molecular Plant Physiology, Max Planck Society;

http://pubman.mpdl.mpg.de/cone/persons/resource/persons97218

Karcher,  D.
Organelle Biology and Biotechnology, Department Bock, Max Planck Institute of Molecular Plant Physiology, Max Planck Society;

http://pubman.mpdl.mpg.de/cone/persons/resource/persons97438

Thiele,  W.
Organelle Biology and Biotechnology, Department Bock, Max Planck Institute of Molecular Plant Physiology, Max Planck Society;

http://pubman.mpdl.mpg.de/cone/persons/resource/persons97077

Bock,  R.
Organelle Biology and Biotechnology, Department Bock, Max Planck Institute of Molecular Plant Physiology, Max Planck Society;

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Citation

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.


Cite as: http://hdl.handle.net/11858/00-001M-0000-0014-2115-8
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.