Magnetic reconnection from a multiscale instability cascade

Magnetic reconnection, the process whereby magnetic field lines break and then reconnect to form a different topology, underlies critical dynamics of magnetically confined plasmas in both nature and the laboratory. Magnetic reconnection involves localized diffusion of the magnetic field across plasma, yet observed reconnection rates are typically much higher than can be accounted for using classical electrical resistivity. It is generally proposed that the field diffusion underlying fast reconnection results instead from some combination of non-magnetohydrodynamic processes that become important on the 'microscopic' scale of the ion Larmor radius or the ion skin depth. A recent laboratory experiment demonstrated a transition from slow to fast magnetic reconnection when a current channel narrowed to a microscopic scale, but did not address how a macroscopic magnetohydrodynamic system accesses the microscale. Recent theoretical models and numerical simulations suggest that a macroscopic, two-dimensional magnetohydrodynamic current sheet might do this through a sequence of repetitive tearing and thinning into two-dimensional magnetized plasma structures having successively finer scales. Here we report observations demonstrating a cascade of instabilities from a distinct, macroscopic-scale magnetohydrodynamic instability to a distinct, microscopic-scale (ion skin depth) instability associated with fast magnetic reconnection. These observations resolve the full three-dimensional dynamics and give insight into the frequently impulsive nature of reconnection in space and laboratory plasmas.     

FACL4, encoding fatty acid-CoA ligase 4, is mutated in nonspecific X-linked mental retardation

X-linked mental retardation (XLMR) is an inherited condition that causes failure to develop cognitive abilities, owing to mutations in a gene on the X chromosome. The latest XLMR update lists up to 136 conditions leading to 'syndromic', or 'specific', mental retardation (MRXS) and 66 entries leading to 'nonspecific' mental retardation (MRX). For 9 of the 66 MRX entries, the causative gene has been identified. Our recent discovery of the contiguous gene deletion syndrome ATS-MR (previously known as Alport syndrome, mental retardation, midface hypoplasia, elliptocytosis, OMIM #300194), characterized by Alport syndrome (ATS) and mental retardation (MR), indicated Xq22.3 as a region containing one mental retardation gene. Comparing the extent of deletion between individuals with ATS-MR and individuals with ATS alone allowed us to define a critical region for mental retardation of approximately 380 kb, containing four genes. Here we report the identification of two point mutations, one missense and one splice-site change, in the gene FACL4 in two families with nonspecific mental retardation. Analysis of enzymatic activity in lymphoblastoid cell lines from affected individuals of both families revealed low levels compared with normal cells, indicating that both mutations are null mutations. All carrier females with either point mutations or genomic deletions in FACL4 showed a completely skewed X-inactivation, suggesting that the gene influences survival advantage. FACL4 is the first gene shown to be involved in nonspecific mental retardation and fatty-acid metabolism.