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UDP‐Glucose level as a limiting factor for IAA‐induced cell elongation in Avena coleoptile segments
Author(s) -
Inouhe Masahiro,
Yamamoto Ryoichi,
Masuda Yoshio
Publication year - 1987
Publication title -
physiologia plantarum
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.351
H-Index - 146
eISSN - 1399-3054
pISSN - 0031-9317
DOI - 10.1111/j.1399-3054.1987.tb01944.x
Subject(s) - coleoptile , avena , elongation , galactose , polysaccharide , chemistry , auxin , sucrose , cell wall , biochemistry , botany , biology , ultimate tensile strength , materials science , gene , metallurgy
The effects of galactose on IAA‐induced elongation and endogenous level of UDP‐glucose (UDPG) in oat ( Avena sativa L. cv. Victory) coleoptile segments were examined under various growth conditions to see if there was a correlation between the level of UDPG and auxin‐induced growth. The following results were obtained:1 Galactose (10 m M ) inhibited the auxin‐induced cell elongation of oat coleoptile segments after a lag of ca 2 h. Determinations of cell wall polysaccharides and UDP‐sugars indicated that galactose, when inhibiting the cell wall polysaccharide synthesis, decreased the level of UDPG but caused an increase in the levels of Gal‐1‐P and UDP‐Gal. 2 When coleoptile segments treated with IAA and galactose were transferred to galactose‐free IAA‐solution, the segment elongation was restored and the amounts of cell wall polysaccharides increased. During this period, the amount of UDPG increased and the levels of Gal‐1‐P and UDP‐Gal slightly decreased or leveled off. The UDP‐pentoses changed similarly as UDPG did. 3 Addition of sucrose (30 m M ) enhanced IAA‐induced cell elongation and removed growth inhibition by 1 m M galactose. Sucrose increased the amounts of the cell wall polysaccharides and the level of UDPG in the presence or absence of IAA and also counteracted the decrease in UDPG caused by galactose.These results indicate that the level of UDPG is an important limiting factor for cell wall biosynthesis and, thus, for auxin‐induced elongation.