J Integr Plant Biol. ›› 2020, Vol. 62 ›› Issue (11): 1741-1761.DOI: 10.1111/jipb.12936

Special Issue: Photosynthesis

• Photosynthesis and Crop Physiology • Previous Articles     Next Articles

Pentatricopeptide repeat protein PHOTOSYSTEM I BIOGENESIS FACTOR2 is required for splicing of ycf3

Xuemei Wang1,2† , Zhipan Yang1,2† , Yi Zhang3 , Wen Zhou1,2, Aihong Zhang3 and Congming Lu3 *   

  1. 1Key Laboratory of Photobiology, Institute of Botany, Chinese Academy of Sciences, Beijing 100093, China
    2College of Life Sciences, University of Chinese Academy of Sciences, Beijing 100049, China
    3State Key Laboratory of Crop Biology, College of Life Sciences, Shandong Agricultural University, Taian 271018, China

    These authors contributed equally to this work
    Email: Congming Lu (cmlu@sdau.edu.cn)
  • Received:2019-12-29 Accepted:2020-03-27 Online:2020-04-06 Published:2020-11-01


To gain a better understanding of the molecular mechanisms of photosystem I (PSI) biogenesis, we characterized the Arabidopsis thaliana photosystem I biogenesis factor 2 (pbf2) mutant, which lacks PSI complex. PBF2 encodes a P‐class pentatricopeptide repeat (PPR) protein. In the pbf2 mutants, we observed a striking decrease in the transcript level of only one gene, the chloroplast gene ycf3, which is essential for PSI assembly. Further analysis of ycf3 transcripts showed that PBF2 is specifically required for the splicing of ycf3 intron 1. Computational prediction of binding sequences and electrophoretic mobility shift assays reveal that PBF2 specifically binds to a sequence in ycf3 intron 1. Moreover, we found that PBF2 interacted with two general factors for group II intron splicing CHLOROPLAST RNA SPLICING2‐ASSOCIATED FACTOR1 (CAF1) and CAF2, and facilitated the association of these two factors with ycf3 intron 1. Our results suggest that PBF2 is specifically required for the splicing of ycf3 intron 1 through cooperating with CAF1 and CAF2. Our results also suggest that additional proteins are required to contribute to the specificity of CAF‐dependent group II intron splicing.

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