In This Issue
People & Ideas
Functional diversity of histone H1 variants may be caused by differences in phosphorylation during interphase.
Defects in lymphangiogenesis are added to the broad clinical manifestations of DiGeorge syndrome, caused by deletion of the T box transcription factor Tbx1.
Mutant huntingtin prevents interaction of the DNA damage repair complex component Ku70 with damaged DNA, blocking repair of double-strand breaks.
Stochastic and reversible assembly of a multiprotein DNA repair complex ensures accurate target site recognition and efficient repair
Computational modeling and quantitative analysis show that although accumulation of repair complexes can take hours, the individual components rapidly exchange between the nucleoplasm and DNA damage sites.
Interpolar microtubules are sorted by the directional instability resulting from antagonistic molecular motors, not a stable balance of force.
LET-99 inhibits lateral posterior pulling forces during asymmetric spindle elongation in C. elegans embryos
GPR-1/2 (regulators of Gα signaling necessary for asymmetric cell division) receives a positional cue from Let-99, resulting in its appropriate distribution around the posterior cortex.
A conserved patch of amino acids in the globular tail of type V myosin binds She3p to localize ASH1 mRNA to the bud of dividing yeast cells.
A component of the rough ER, SUN domain protein osteopotentia, regulates expansion of this organelle in osteoblasts during skeletal development and regeneration.
Apo2 proteins interact with chaperone Unc45b (but not Hsp90) and are required for correct zebrafish skeletal musculature and heart function.
Microtubules and intermediate filaments cooperate with actin and other components of filopodia during invadopodia maturation.
A two-tiered mechanism of EGFR inhibition by RALT/MIG6 via kinase suppression and receptor degradation
The EGFR kinase inhibitor RALT/MIG6 also functions as an endocytic adaptor to promote receptor internalization by scaffolding AP-2 and intersectins.
β-Arrestin–dependent activation of Ca2+/calmodulin kinase II after β1–adrenergic receptor stimulation
β-Arrestin functions as a scaffold for CaMKII and the Rap guanine nucleotide exchange factor Epac to regulate signaling from β1-ARs.
Synaptic persistence is enhanced by N-cadherin, which clusters together in response to neural activity and long-term potentiation induction in dendritic spines.
A complex that localizes to the C1d central pair projection of cilia controls flagellar waveform and beat frequency in response to calcium.