Mutation at the chlamydomonas nuclear NAC2 locus specifically affects stability of the chloroplast psbD transcript encoding polypeptide D2 of PS II

• Published in: Cell Vol. 58; no. 5; pp. 869 - 876
• Main Authors: Kuchka, M.R., Goldschmidt-Clermont, M., van Dillewijn, J., Rochaix, J.-D.
• Format: Journal Article
• Language: English
• Published: Cambridge, MA Elsevier Inc 08.09.1989; Cell Press
• Subjects: Biological and medical sciences; Chlamydomonas - genetics; Chlorophyll - genetics; Chloroplasts - physiology; Classical genetics, quantitative genetics, hybrids; Fundamental and applied biological sciences. Psychology; Gene Expression Regulation; Genes; Genetics of eukaryotes. Biological and molecular evolution; Light-Harvesting Protein Complexes; Mutation; Photosynthetic Reaction Center Complex Proteins; Photosystem II Protein Complex; Plant Proteins - genetics; RNA Processing, Post-Transcriptional; RNA, Messenger - metabolism; Thallophyta, bryophyta; Transcription, Genetic; Vegetals; Molecular processing; Stability; Splicing; Gene interaction; Gene product; Chloroplast DNA; Nucleocytoplasmic interaction; Thylakoid; Northern blotting; Autoradiography; Photosystem 2; Messenger RNA; Immunoblotting assay; Trans acting regulatory factor; Mutation; Chloroplast
• ISSN: 0092-8674; 1097-4172
• DOI: 10.1016/0092-8674(89)90939-2

The nuclear NAC2 locus of C. reinhardtii encodes a trans-acting factor that confers stability on the chloroplast message for the D2 protein of photosystem II (PS II). A mutant that carries a lesion in the NAC2 gene is unable to accumulate the psbD transcript encoding D2, but synthesizes all other PS II proteins normally. However, the PS II complex is completely unstable in the nac2–26 mutant, and all major PS II polypeptides, including the three oxygen-evolving enhancing proteins, are absent or greatly reduced in this strain because of posttranslational degradation. In C. reinhardtii the second exon of the trans-spliced psaA mRNA is cotranscribed with psbD (Choquet et al., 1988), but the nac2–26 mutation normally has no effect on psaA message maturation or stability. However, in double mutants carrying the nac2–26 mutation, as well as a mutation that prevents psaA splicing, splicing intermediates carrying psbD sequences are degraded. These results suggest that the NAC2 gene product acts in a very specific manner to control the half-life of psbD transcripts.