New SHRIMP zircon and monazite 206 Pb/ 238 U and 208 Pb/ 232 Th ages on structurally controlled units and 40 Ar- 39 Ar step-heating ages from shear fabrics, define three distinct regional tectonic events in the southern Sierras Pampeanas. The first, the Pampean orogeny, involved closure of a late Neoproterozoic basin on the western margin of Gondwana. New rims on detrital zircons and concurrent monazite growth suggest that the metamorphic peak was attained by c. 530 Ma. The second event, the Famatinian orogeny, marks the initiation of eastward-dipping subduction on the western Gondwana margin, and may represent a continuation of the earlier Pampean event. Metasedimentary rocks from the Sierras de San Luis have zircons with a predominantly Early Cambrian detrital age, indicating a Pampean source. The metamorphic peak in these rocks was contemporaneous with the emplacement of felsic, mafic and ultramafic rocks at c. 480 Ma in a collisional setting. Monazite ages and limited new zircon growth in the metasedimentary rocks suggest that the Famatinian orogeny had ceased by about 450 Ma. This correlates well with a 450–460 Ma Ar-Ar age for late shearing in the southern sierras of La Rioja province. The third tectonic event, the Achalian orogeny, involved W-directed compression and emplacement of multiple, voluminous, granite intrusions. Deformation during this event was partitioned between discrete shear-zones and regions of open to tight folding. The shear zones alternate between W-directed thrusts and NNW-trending, sinistral shear-zones. Ar-Ar data from the low-grade shear fabrics indicate that transpressional deformation continued through most of the Devonian.

Synaptobrevin-like membrane proteins that reside on transport vesicles, called the vesicle SNARE (v-SNARE), play a key role in ensuring that a vesicle targets and fuses with its correct acceptor compartment. Here we show that Bos1p, the v-SNARE of yeast endoplasmic reticulum-to-Golgi transport vesicles, pairs with another integral membrane protein of similar topology (Sec22p) on vesicles. This pairing, which appears to require functional Ypt1p (Rab in mammalian cells), may aid the activity of Bos1p on this compartment. These findings suggest that Rabs regulate the specificity of membrane fusion by selectively activating the v-SNARE on carrier vesicles. Because the v-SNARE resides on more than one membrane, such a regulated activation step may be necessary to prevent the premature fusion of donor and acceptor compartments.

One of the most prominent but least understood demographic phenomena in the precontact Southwest is the disappearance of the Hohokam from the valleys of southern Arizona. Despite extensive research, no widely accepted explanation has been offered. We argue that the failure to identify a satisfactory cause is due to excessive focus on catastrophic phenomena and terminal occupations, and a lack of attention to gradual demographic processes. Based on a combination of macro-regional population studies and local research in the lower San Pedro River valley, we present an explanation for gradual population decline precipitated by social and economic coalescence beginning in the late A.D. 1200s. In the southern Southwest an influx of immigrants from the north led to a shift from a dispersed, extensive settlement/subsistence strategy to increased conflict, aggregation, and economic intensification. This shift resulted in diminished health and transformation from population growth to decline. Over approximately 150 years gradual population decline resulted in small remnant groups unable to maintain viable communities. Small, terminal populations were ultimately unable to continue identifiable Hohokam cultural traditions and consequently disappeared from the archaeological record of southern Arizona, either through migration or a shift in lifestyle that rendered them archaeologically invisible.

The cytoplasmic protein tyrosine phosphatase, PTP-PEST, associates with the focal adhesion proteins p130cas and paxillin and has recently been implicated in cell migration. In this study, we investigated the mechanism by which PTP-PEST regulates this phenomenon. We find that PTP-PEST is activated in an adhesion-dependent manner and localizes to the tips of membrane protrusions in spreading fibroblasts. We show that the catalytic activity of PTP-PEST is a key determinant for its effects on motility. Overexpression of PTP-PEST, but not a catalytically inactive form, impairs haptotaxis, cell spreading and formation of membrane protrusions in CHOK1 cells. In addition, overexpression of PTP-PEST in Rat1 fibroblasts perturbs membrane ruffling and motility in response to PDGF stimulation. The expression level of PTP-PEST modulates the activity of the small GTPase, Rac1. PTP-PEST overexpression suppresses activation of Rac1 in response to both integrin-mediated adhesion or growth factor stimulation. In contrast, fibroblasts that lack PTP-PEST expression show enhanced Rac1 activity. Co-expression of constitutively active Rac1 with PTP-PEST overcomes the inhibition of cell spreading and migration indicating that PTP-PEST acts by antagonizing Rac1 activation. Our data suggest a model in which PTP-PEST is activated by integrins and localized to regions where it can control motile events at the leading edge through inhibition of the small GTPase Rac1.