Seed germination is antagonistically controlled by the phytohormones gibberellic acid (GA) and abscisic acid (ABA). GA promotes seed germination by enhancing the proteasome-mediated destruction of RGL2 (for RGA-LIKE2), a key DELLA factor repressing germination. By contrast, ABA blocks germination by inducing ABI5 (for ABA-INSENSITIVE5), a basic domain/leucine zipper transcription factor repressing germination. Decreased GA synthesis leads to an increase in endogenous ABA levels through a stabilized RGL2, a process that may involve XERICO, a RING-H2 zinc finger factor promoting ABA synthesis. In turn, increased endogenous ABA synthesis is necessary to elevate not only ABI5 RNA and protein levels but also, critically, those of RGL2. Increased ABI5 protein is ultimately responsible for preventing seed germination when GA levels are reduced. However, overexpression of ABI5 was not sufficient to repress germination, as ABI5 activity requires phosphorylation. The endogenous ABI5 phosphorylation and inhibition of germination could be recapitulated by the addition of a SnRK2 protein kinase to the ABI5 overexpression line. In sleepy1 mutant seeds, RGL2 overaccumulates; germination of these seeds can occur under conditions that produce low ABI5 expression. These data support the notion that ABI5 acts as the final common repressor of germination in response to changes in ABA and GA levels.

Several Arabidopsis mutants have been isolated that either bypass this ABA-mediated growth arrest or show an enhanced response to ABA (for review, see Finkelstein et al. 2002). The latter category includes mutations in ERA1, which encodes a subunit of a farnesyl transferase (Cutler et al. 1996), and ABH1, which encodes a mRNA cap binding protein (Hugouvieux et al. 2001). Mutants bypassing the ABA-mediated growth inhibition were designated abi1, abi2, abi3, abi4, abi5, abi8 (for ABAinsensitive), cho1, and cho2 (Koornneef et al. 1984;Finkelstein 1994;Lopez-Molina and Chua 2000;Finkelstein et al. 2002;Nambara et al. 2002). The ABI8, CHO1, and CHO2 genes have not yet been cloned Nambara et al. 2002). ABI1 and ABI2 encode two homologous serine/threonine phosphatases of class 2C (Leung et al. 1994(Leung et al. , 1997Meyer et al. 1994;Rodriguez et al. 1998), and both abi1 and abi2 have identical Gly-

A redox neutral, highly enantioselective coupling between N-arylaminomethanes and N-sulfonyl aldimines was developed by harnessing the efficient catalysis of P-spiro chiral arylaminophosphonium barfate and a transition-metal photosensitizer under visible light irradiation. This mode of synergistic catalysis provides a powerful strategy for controlling the bond-forming processes of reactive radical intermediates.

The functions of microRNAs and their target mRNAs in Arabidopsis thaliana development have been widely documented; however, roles of stress-responsive microRNAs and their targets are not as well understood. Using small RNA deep sequencing and ATH1 microarrays to profile mRNAs, we identified IAA-Ala Resistant3 (IAR3) as a new target of miR167a. As expected, IAR3 mRNA was cleaved at the miR167a complementary site and under high osmotic stress miR167a levels decreased, whereas IAR3 mRNA levels increased. IAR3 hydrolyzes an inactive form of auxin (indole-3-acetic acid [IAA]-alanine) and releases bioactive auxin (IAA), a central phytohormone for root development. In contrast with the wild type, iar3 mutants accumulated reduced IAA levels and did not display high osmotic stress-induced root architecture changes. Transgenic plants expressing a cleavage-resistant form of IAR3 mRNA accumulated high levels of IAR3 mRNAs and showed increased lateral root development compared with transgenic plants expressing wild-type IAR3. Expression of an inducible noncoding RNA to sequester miR167a by target mimicry led to an increase in IAR3 mRNA levels, further confirming the inverse relationship between the two partners. Sequence comparison revealed the miR167 target site on IAR3 mRNA is conserved in evolutionarily distant plant species. Finally, we showed that IAR3 is required for drought tolerance.