The apical hook is a structure that allows the seedling to penetrate through soil without damaging the fragile cotyledons. Its formation requires unequal cell expansions at the convex and concave sides of the hook, respectively. It has been shown that TMK1 is involved in both cell expansion and repression of cell expansion through two different pathways on either side. On the developing convex side, low levels of auxin lead to the phosphorylation and thus activation of proton pumps by TMK1, thereby inducing cell wall acidification, which is necessary for cell expansion. On the concave side, however, higher levels of auxin lead to the C-terminal cleavage of TMK1, with the TMK1C fragment translocating into the nucleus and inhibiting cell expansion by phosphorylation of two Aux/IAA proteins: IAA32 and IAA34.
These researchers show that the family of DA1 peptidases is responsible for TMK1 cleavage and is required for repression of cell expansion and thus apical hook formation. DA1, as well as the DA1-related proteins DAR1 and DAR2, could cleave TMK1 at the predicted site, with DAR2 having the highest in vitro activity but with DAR1 likely being the peptidase responsible for in vivo cleavage. Only dar1 mutants had an open apical hook, and DAR1 is expressed in the apical hook region, while DA1 and DAR2 are expressed in the vasculature instead. The apical hook phenotype of the tmk1 mutant could be complemented by expression of the TMK1C fragment under an auxin-responsive promoter alone, while replacement of the DA1-family cleavage site with a non-cleavable sequence failed to complement. The fact that DA1 and DAR2 are expressed in the vasculature poses the question whether a similar TMK1C-dependent pathway could be involved in vasculature development as well.
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