The parsec-scale jet in M87.

We briefly review the observed structure and evolution of the M87 jet on scales less, similar1 parsec (pc; 1 pc = 3.09 x 10(16) m). Filamentary features, limb-brightening, and side-to-side oscillation are common characteristics of the pc-scale, and kpc-scale jets. The most prominent emission features on both the pc and subpc scales appear stationary (v/c < 0.1). Nonetheless, based on the jet's flux evolution, the presence of kpc-scale superluminal motion, and the absence of a visible counter-jet, we argue for the presence of an underlying relativistic flow, consistent with unified models. The initial jet collimation appears to occur on scales <0.1 pc, thus favoring electromagnetic processes associated with a black hole and accretion disk.

The nuclear jet and counterjet region of the radio galaxy Cygnus A.

Very-long-baseline interferometry images of the nuclear region of the radio galaxy Cygnus A reveal a pronounced "core" and a knotty jet and counterjet. The knots are moving away from the core at apparent speeds which are subluminal for h = 1 [h = H0/100 km.s-1.Mpc-1;1 parsec (pc) = 3.09 x 10(16)m] and about c for h = 0.5. The jet is aligned with the outer, kiloparsec-scale jet to within 2 degrees. The counterjet has a total flux density at 5 GHz of about one-fifth of that of the jet. In the context of the twin relativistic jet model for active galactic nuclei, the jet in Cygnus A is oriented at an angle to our line of sight of 35-80 degrees and 55-85 degrees, and the intrinsic velocity of the jet fluid is 0.4-0.6c and 0.6-1c for h = 1 and h = 0.5, respectively.

APX-1 can substitute for its homolog LAG-2 to direct cell interactions throughout Caenorhabditis elegans development.

The homologous LAG-2 and APX-1 membrane proteins are putative signaling ligands in the GLP-1/LIN-12 signal-transduction pathway in Caenorhabditis elegans. Normally, LAG-2 and APX-1 mediate distinct cell interactions. Here, we demonstrate that APX-1, which normally interacts with GLP-1 in the early embryo, can substitute for LAG-2 throughout development. When expressed under control of the lag-2 promoter, an apx-1 cDNA can completely rescue a lag-2 null mutant. To substitute for LAG-2, APX-1 must be able to interact with both GLP-1 and LIN-12 receptors and to mediate a variety of cell interactions during development. Therefore, APX-1 and LAG-2 are essentially equivalent in their ability to influence receptor activity. On the basis of this result, we suggest that the existence of multiple-signaling ligands in the LIN-12/GLP-1 signal transduction pathway does not reflect the evolution of functionally distinct proteins but rather the imposition of distinct controls of gene expression upon functionally similar proteins. Finally, we propose that the specification of distinct cell fates by the LIN-12/GLP-1 signal-transduction pathway relies on activities functioning downstream of the ligand and receptor, rather than on specific ligand-receptor interactions.