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Plant and Cell Physiology, 2004, Vol. 45, No. 6 781-788
© 2004 Oxford University Press

Knock-out of the Plastid Ribosomal Protein S21 Causes Impaired Photosynthesis and Sugar-Response during Germination and Seedling Development in Arabidopsis thaliana

Chizuko Morita-Yamamuro1, Tomokazu Tsutsui1, Ayumi Tanaka2 and Junji Yamaguchi1,3

1 Division of Biological Sciences, Graduate School of Science, Hokkaido University, Kita-ku N10-W8, Sapporo, 060-0810 Japan
2 Institute of Low Temperature Science, Hokkaido University, Kita-ku N19-W8, Sapporo, 060-0819 Japan

To clarify the mechanism of sugar-response of higher plants, the ghs1 (glucose hypersensitive) mutant of Arabidopsis was isolated and characterized. The ghs1 mutant had an increased sensitivity to glucose, showing a dramatic inhibition of chlorophyll synthesis and developmental arrest of leaves when grown on medium containing more than 5% glucose; the wild type required exposure to 7% glucose to show the same response. The ghs1 mutant is a single recessive loss-of-function mutation caused by a T-DNA insertion in the GHS1 gene (At3g27160), which encodes the plastid 30S ribosomal protein S21. The mutant showed: (1) reduction in the translation product but not the transcript for plastid-encoded rbcL, (2) reduction in photosynthetic activity monitored with pulse-amplitude modulated fluorometry, (3) impaired chloroplast development, as observed by electron microscopy. These results indicate that the deficiency of such chloroplast functions as photosynthetic activity observed in the ghs1 mutant is caused by impaired plastid protein synthesis associated with loss of ribosomal S21 protein. Relationships between the GHS1 gene and sugar-response are discussed.

3 Corresponding author: E-mail, jjyama{at}sci.hokudai.ac.jp; Fax, +81-11-706-2737.


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