Localization and the interface between quantum mechanics, quantum field theory and quantum gravity II: The search of the interface between QFT and QG

The main topics of this second part of a two-part essay are some consequences of the phenomenon of vacuum polarization as the most important physical manifestation of modular localization. Besides philosophically unexpected consequences, it has led to a new constructive “outside-inwards approach” in which the pointlike fields and the compactly localized operator algebras which they generate only appear from intersecting much simpler algebras localized in noncompact wedge regions whose generators have extremely mild almost free field behavior.Another consequence of vacuum polarization presented in this essay is the localization entropy near a causal horizon which follows a logarithmically modified area law in which a dimensionless area (the area divided by the square of dR where dR is the thickness of a light-sheet) appears. There are arguments that this logarithmically modified area law corresponds to the volume law of the standard heat bath thermal behavior. We also explain the symmetry enhancing effect of holographic projections onto the causal horizon of a region and show that the resulting infinite dimensional symmetry groups contain the Bondi–Metzner–Sachs group. This essay is the second part of a partitioned longer paper.     

A vertebrate actin-related protein is a component of a multisubunit complex involved in microtubule-based vesicle motility.

Actin is a cytoskeletal protein which is highly conserved across eukaryotic phyla. Actin filaments, in association with a family of myosin motor proteins, are required for cellular motile processes as diverse as vesicle transport, cell locomotion and cytokinesis. Many organisms have several closely related actin isoforms. In addition to conventional actins, yeasts contain actin-related proteins that are essential for viability. We show here that vertebrates also contain an actin-related protein (actin-RPV). Actin-RPV is a major component of the dynactin complex, an activator of dynein-driven vesicle movement, indicating that unlike conventional actins which work in conjunction with myosin motors, actin-RPV may be involved in cytoplasmic movements via a microtubule-based system.     

Localization of cytoplasmic dynein to mitotic spindles and kinetochores

What is the origin of the forces generating chromosome and spindle movements in mitosis? Both microtubule dynamics and microtubule-dependent motors have been proposed as the source of these motor forces. Cytoplasmic dynein and kinesin are two soluble proteins that power membranous organelle movements on microtubules. Kinesin directs movement of organelles to the 'plus' end of microtubules, and is found at the mitotic spindle in sea urchin embryos, but not in mammalian cells. Cytoplasmic dynein translocates organelles to the 'minus' end of microtubules, and is composed of two heavy chains and several light chains. We report here that monoclonal antibodies to two of these subunits and to another polypeptide that associates with dynein localize the protein to the mitotic spindle and to the kinetochores of isolated chromosomes, suggesting that cytoplasmic dynein is important in powering movements of the spindle and chromosomes in dividing cells.     

A recurrent 15q13.3 microdeletion syndrome associated with mental retardation and seizures

We report a recurrent microdeletion syndrome causing mental retardation, epilepsy and variable facial and digital dysmorphisms. We describe nine affected individuals, including six probands: two with de novo deletions, two who inherited the deletion from an affected parent and two with unknown inheritance. The proximal breakpoint of the largest deletion is contiguous with breakpoint 3 (BP3) of the Prader-Willi and Angelman syndrome region, extending 3.95 Mb distally to BP5. A smaller 1.5-Mb deletion has a proximal breakpoint within the larger deletion (BP4) and shares the same distal BP5. This recurrent 1.5-Mb deletion contains six genes, including a candidate gene for epilepsy (CHRNA7) that is probably responsible for the observed seizure phenotype. The BP4-BP5 region undergoes frequent inversion, suggesting a possible link between this inversion polymorphism and recurrent deletion. The frequency of these microdeletions in mental retardation cases is approximately 0.3% (6/2,082 tested), a prevalence comparable to that of Williams, Angelman and Prader-Willi syndromes.