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Vol. 15, No. 7, pp. 902-911, April 1, 2001
1 Department of Biology, The University of North Carolina
at Chapel Hill, Chapel Hill, North Carolina 27599, USA; 2 Cell
and Molecular Biology Program and the Department of Horticulture,
University of Wisconsin, Madison, Wisconsin 53706, USA
To directly address the function of a putative auxin receptor
designated ABP1, a reverse genetic approach was taken to identify and
characterize ABP1 mutant alleles in Arabidopsis. A
homozygous null mutation in ABP1 confers embryo lethality. Null
mutant embryos develop normally until the early stages of the globular
embryo but are unable to make the transition to a bilaterally
symmetrical structure because cells fail to elongate. Cell division was
also aberrant both in the suspensor and embryo proper. Antisense
suppression of ABP1 in tobacco cells causes slow proliferation
and eliminates auxin-induced cell elongation and reduces cell division.
The complete lack of auxin-inducible elongation in individual cells
confirms the results observed in embryos, indicates a cell autonomous
function, and, taken together with biochemical evidence that ABP1 binds auxins, suggests that ABP1 mediates auxin-induced cell elongation and,
directly or indirectly, cell division.
[Key Words: Auxin; auxin-binding protein 1; embryogenesis; BY-2; cell elongation; cell division]
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