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Abstract

At early stages of Arabidopsis embryogenesis, the timely accumulation of phytohormone auxin in the
future vasculature causes degradation of the Aux/IAA inhibitor BDL/IAA12. This releases the ARF
transcription factor MP/ARF5, resulting in root meristem initiation via TMO7 expression and
presumably PIN1-dependent directional auxin transport. Loss of MP activity, stabilization of BDL, or
overexpression of AGCVIII protein kinases leads to failure of root meristem initiation and
subsequently seedlings without a primary root.
In a complementary experimental approach to test for the negative regulatory importance of
Aux/IAA proteins, embryonic expression of both an auxin-insensitive MP (MPΔPB1) and a nonrepressive,
stabilized BDL (BDLmIIΔDI) also interfered with root meristem initiation. Overexpression
of AGCVIII kinases like PINOID causes a rootless phenotype comparable to that of MPΔPB1 and
BDLmIIΔDI.
We show that loss of the embryonic root caused by both auxin-insensitive MP as well as nonrepressive,
stabilized BDL can be suppressed by reducing the dosage of PINOID kinase. As embryonic
expression of PID had been reported to change the polar localization of auxin efflux carrier PIN1 from
basal to apical, we analyzed the subcellular localization of PIN1 in early embryogenesis and found it
unchanged in embryos expressing MPΔPB1, BDLmIIΔDI, and PID. To elucidate the underlying
signaling mechanisms of embryonic root meristem initiation, we currently are testing both
downstream targets of MP in the earliest embryonic stages and are trying to connect these with
phosphorylation targets of the PINOID kinase. Our results support a model in which the auxin
response module MP-BDL represses PID and other AGCVIII kinases, giving rise to proper root initiation.