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Plant Physiol, March 2002, Vol. 128, pp. 812-821
Adenosine Kinase Deficiency Is Associated with Developmental
Abnormalities and Reduced Transmethylation1
Barbara A.
Moffatt,*
Yvonne Y.
Stevens,2
Michael S.
Allen,
Jamie D.
Snider,3
Luiz A.
Pereira,
Margarita I.
Todorova,
Peter S.
Summers,
Elizabeth A.
Weretilnyk,
Luke
Martin-McCaffrey,4 and
Conrad
Wagner
Department of Biology, University of Waterloo, Waterloo, Ontario,
Canada N2L 3G1 (B.A.M., Y.Y.S., M.S.A., J.D.S., L.A.P., M.I.T.,
L.M.-M.); Department of Biology, McMaster University, Hamilton,
Ontario, Canada L8S 4K1 (P.S.S., E.A.W.); and Department of
Biochemistry, Vanderbilt University School of Medicine, and Department
of Veterans Health Care System, Nashville Campus, Vanderbilt
University, Nashville, Tennessee 37232 (C.W.)
Adenosine (Ado) kinase (ADK; ATP:Ado 5' phosphotransferase,
EC 2.7.1.20) catalyzes the salvage synthesis of adenine monophosphate from Ado and ATP. In Arabidopsis, ADK is encoded by two cDNAs that
share 89% nucleotide identity and are constitutively, yet differentially, expressed in leaves, stems, roots, and flowers. To
investigate the role of ADK in plant metabolism, lines deficient in
this enzyme activity have been created by sense and antisense expression of the ADK1 cDNA. The levels of ADK activity
in these lines range from 7% to 70% of the activity found in
wild-type Arabidopsis. Transgenic plants with 50% or more of the
wild-type activity have a normal morphology. In contrast, plants with
less than 10% ADK activity are small with rounded, wavy leaves and a
compact, bushy appearance. Because of the lack of elongation of the
primary shoot, the siliques extend in a cluster from the rosette.
Fertility is decreased because the stamen filaments do not elongate
normally; hypocotyl and root elongation are reduced also. The
hydrolysis of S-adenosyl-L-homo-cysteine
(SAH) produced from S-adenosyl-L-methionine
(SAM)-dependent methylation reactions is a key source of Ado in plants.
The lack of Ado salvage in the ADK-deficient lines leads to an increase
in the SAH level and results in the inhibition of SAM-dependent
transmethylation. There is a direct correlation between ADK activity
and the level of methylesterified pectin in seed mucilage, as monitored
by staining with ruthenium red, immunofluorescence labeling, or direct
assay. These results indicate that Ado must be steadily removed by ADK to prevent feedback inhibition of SAH hydrolase and maintain SAM utilization and recycling.
1
This work was supported by the Natural Sciences
and Engineering Research Council of Canada (research grants to B.A.M.
and E.A.W.), by the Public Health Service (grant nos. DK15289 and DK54859 to C.W.), and by the Office of Research and Development, Medical Research Service, Department of Veterans Affairs (Merit Revue
award to C.W.).
2
Present address: Regional Primate Research Center,
University of Washington, Box 357330, Seattle, WA 98195-7330.
3
Present address: Department of Biochemistry, University
of Toronto, Toronto, ON, Canada M5S 1A1.
4
Present address: Department of Pharmacology and
Toxicology, Medical Sciences Building, University of Western
Ontario, London, Ontario, Canada N6A 5C1.
*
Corresponding author; email moffatt{at}sciborg.uwaterloo.ca; fax
519-746-0614.
© 2002 American Society of Plant Physiologists
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