SOMATIC HYBRIDIZATION WITH APHOTOTROPIC MUTANTS OF THE MOSS CERATODONPURPUREUS - GENOME SIZE, PHYTOCHROME PHOTOREVERSIBILITY, TIP-CELL PHOTOTROPISM AND CHLOROPHYLL REGULATION

Citation
T. Lamparter et al., SOMATIC HYBRIDIZATION WITH APHOTOTROPIC MUTANTS OF THE MOSS CERATODONPURPUREUS - GENOME SIZE, PHYTOCHROME PHOTOREVERSIBILITY, TIP-CELL PHOTOTROPISM AND CHLOROPHYLL REGULATION, Journal of plant physiology, 153(3-4), 1998, pp. 394-400
Citations number
19
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Plant Sciences
Journal title
ISSN journal
0176-1617
Volume
153
Issue
3-4
Year of publication
1998
Pages
394 - 400
Database
ISI
SICI code
0176-1617(1998)153:3-4<394:SHWAMO>2.0.ZU;2-T
Abstract
This paper describes somatic fusion of protoplasts in the moss Ceratod on purpureus, specifically of the phototropic mutants ptr103 and ptr11 6. Phototropism of Ceratodon filaments is phytochrome mediated. The pt r116 mutant is thought to carry a lesion in the biosynthetic pathway o f the phytochrome chromophore; this mutant grows negatively gravitropi cally in continuous unilateral red light. The ptr103 mutation is thoug ht to effect phytochrome signal transduction: the phenotype of this mu tant is clearly distinguishable from wildtype and ptr116 because filam ents grow in random directions in continuous unilateral red. Following protoplasting and PEG-mediated protoplast fusion with ptr103 and ptr1 16, lines with a wildtype-like phenotype were identified, propagated a nd tested for genome size and phytochrome physiology. The 1C genome si ze of Ceratodon is estimated to lie between 240 and 270 Mbp, based on comparisons with Arabidopsis thaliana (genome size 100 Mbp). The genom e size of one line that arose from a fusion experiment, Ptr103(+)ptr11 6, was shown by flow cytometry to be ca. twice that of the wildtype. W ith respect to phytochrome spectral activity, phototropism and regulat ion of chlorophyll synthesis, ptr103(+)ptr116 was similar to the wildt ype. These data are consistent with ptr103(+)ptr116 being a bona fide somatic fusion product in which each mutant parent complements a reces sive genetic lesion of the other.