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Treatment of an anionic dimanganaborylene complex ([{Cp(CO)\(_2\)Mn}\(_2\)B]\(^-\)) with coinage metal cations stabilized by a very weakly coordinating Lewis base (SMe\(_2\)) led to the coordination of the incoming metal and subsequent displacement of dimethylsulfide in the formation of hexametalladiborides featuring planar four-membered M\(_2\)B\(_2\) cores (M = Cu, Au) comparable to transition metal clusters constructed around four-membered rings composed solely of coinage metals. The analogies between compounds consisting of B\(_2\)M\(_2\) units and M\(_4\) (M = Cu, Au) units speak to the often overlooked metalloid nature of boron. Treatment of one of these compounds (M = Cu) with a Lewis-basic metal fragment (Pt(PCy\(_3\))\(_2\)) led to the formation of a tetrametallaboride featuring two manganese, one copper and one platinum atom, all bound to boron in a geometry not yet seen for this kind of compound. Computational examination suggests that this geometry is the result of d\(^{10}\)-d\(^{10}\) dispersion interactions between the copper and platinum fragments.
In the molecular structure of the dinuclear title compound \([η^5-(C_5(CH_3)_5)(CO)Fe{(μ-BCl)(μ-CO)}PtCl(P(C_6H_{11})_3)]·C_6H_6\), the two metal atoms, iron(II) and platinum(II), are bridged by one carbonyl (μ-CO) and one chloridoborylene ligand (μ-BCl). The \(Pt^{II}\) atom is additionally bound to a chloride ligand situated trans to the bridging borylene, and a tricyclohexylphosphane ligand \((PCy_3)\) trans to the carbonyl ligand, forming a distorted square-planar structural motif at the \(Pt^{II}\) atom. The \(Fe_{II}\) atom is bound to a pentamethylcyclopentadienyl ligand \([η^5-C_5(CH_3)_5]\) and one carbonyl ligand (CO), forming a piano-stool structure. Additionally, one benzene solvent molecule is incorporated into the crystal structure, positioned staggered relative to the pentamethylcyclopentadienyl ligand at the \(Fe^{II}\) atom, with a centroid–centroid separation of 3.630 (2) Å.
Meiotic chromosome movement is important for the pairwise alignment of homologous chromosomes, which is required for correct chromosome segregation. Movement is driven by cytoplasmic forces, transmitted to chromosome ends by nuclear membrane-spanning proteins. In animal cells, lamins form a prominent scaffold at the nuclear periphery, yet the role lamins play in meiotic chromosome movement is unclear. We show that chromosome movement correlates with reduced lamin association with the nuclear rim, which requires lamin phosphorylation at sites analogous to those that open lamina network crosslinks in mitosis. Failure to remodel the lamina results in delayed meiotic entry, altered chromatin organization, unpaired or interlocked chromosomes, and slowed chromosome movement. The remodeling kinases are delivered to lamins via chromosome ends coupled to the nuclear envelope, potentially enabling crosstalk between the lamina and chromosomal events. Thus, opening the lamina network plays a role in modulating contacts between chromosomes and the nuclear periphery during meiosis.