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A new iron aziridination catalyst supported by a macrocyclic tetracarbene ligand has been synthesized. The catalyst, [((Me,Et)TC(Ph))Fe(NCCH(3))(2)](PF(6))(2), was synthesized from the tetraimidazolium precursor ((Me,Et)TC(Ph))(I)(4) and characterized by NMR spectroscopy, electrospray ionization mass spectrometry, and single-crystal X-ray diffraction. This iron complex catalyzes the aziridination of electron-donating aryl azides and a wide variety of substituted aliphatic alkenes, including tetrasubstituted ones, in a "C(2) + N(1)" addition reaction. Finally, the catalyst can be recovered and reused up to three additional times without significant reduction in yield.

We have prepared a series of divalent cobalt(II) complexes supported by the [PhBP3] ligand ([PhBP3] = [PhB(CH2PPh2)3]-) to probe certain structural and electronic phenomena that arise from this strong field, anionic tris(phosphine) donor ligand. The solid-state structure of the complex [PhBP3]CoI (1), accompanied by SQUID, EPR, and optical data, indicates that it is a pseudotetrahedral cobalt(II) species with a doublet ground statethe first of its type. To our knowledge, all previous examples of 4-coordinate cobalt(II) complexes with doublet ground states have adopted square planar structure types. Complex 1 provided a useful precursor to the corresponding bromide and chloride complexes, {[PhBP3]Co(μ-Br)}2, (2), and {[PhBP3]Co(μ-Cl)}2, (3). These complexes were similarly characterized and shown to be dimeric in the solid-state. In solution, however, the monomeric low spin form of 2 and 3 dominates at 25 °C. There is spectroscopic evidence for a temperature-dependent monomer/dimer equilibrium in solution for complex 3. Furthermore, the dimers 2 and 3 did not display appreciable antiferromagnetic coupling that is typical of halide and oxo-bridged copper(II) and cobalt(II) dimers. Rather, the EPR and SQUID data for solid samples of 2 and 3 suggest that they have triplet ground states. Complexes 1, 2, and 3 are extremely oxygen sensitive. Thus, stoichiometric oxidation of 1 by dioxygen produced the 4-coordinate, high spin complex [PhB(CH2P(O)Ph2)2(CH2PPh2)]CoI, (4), in which the [PhBP3] ligand had undergone a 4-electron oxidation. Reaction of 1 with TlOAr (Ar = 2,6-Me2Ph) afforded an example of a 4-coordinate, high spin complex, [PhBP3]Co(O-2,6-Me2Ph) (5), with an intact [PhBP3] ligand. The latter two complexes were spectroscopically and structurally characterized for comparison to complexes 1, 2, and 3. Our data for these complexes collectively suggest that the [PhBP3] ligand provides an unusually strong ligand-field to these divalent cobalt complexes that is chemically distinct from typical tris(phosphine) donor ligand sets, and distinct from tridentate borato ligands that have been previously studied. Coupling this strong ligand-field with a pronounced axial distortion away from tetrahedral symmetry, a geometric consequence that is enforced by the [PhBP3] ligand, provides access to monomeric [PhBP3]CoX complexes with doublet rather than quartet ground states.

Checkpoints maintain order and fidelity in the cell cycle by blocking late-occurring events when earlier events are improperly executed. Here we describe evidence for the participation of Chk1 in an intra-S phase checkpoint in mammalian cells. We show that both Chk1 and Chk2 are phosphorylated and activated in a caffeine-sensitive signaling pathway during S phase, but only in response to replication blocks, not during normal S phase progression. Replication block–induced activation of Chk1 and Chk2 occurs normally in ataxia telangiectasia (AT) cells, which are deficient in the S phase response to ionizing radiation (IR). Resumption of synthesis after removal of replication blocks correlates with the inactivation of Chk1 but not Chk2. Using a selective small molecule inhibitor, cells lacking Chk1 function show a progressive change in the global pattern of replication origin firing in the absence of any DNA replication. Thus, Chk1 is apparently necessary for an intra-S phase checkpoint, ensuring that activation of late replication origins is blocked and arrested replication fork integrity is maintained when DNA synthesis is inhibited.

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