Magnetotelluric exploration has shown that the middle and lower crust is anomalously conductive across most of the north-to-south width of the Tibetan plateau. The integrated conductivity (conductance) of the Tibetan crust ranges from 3000 to greater than 20,000 siemens. In contrast, stable continental regions typically exhibit conductances from 20 to 1000 siemens, averaging 100 siemens. Such pervasively high conductance suggests that partial melt and/or aqueous fluids are widespread within the Tibetan crust. In southern Tibet, the high-conductivity layer is at a depth of 15 to 20 kilometers and is probably due to partial melt and aqueous fluids in the crust. In northern Tibet, the conductive layer is at 30 to 40 kilometers and is due to partial melting. Zones of fluid may represent weaker areas that could accommodate deformation and lower crustal flow.

Hsp100 family chaperones of microorganisms and plants cooperate with the Hsp70/Hsp40/NEF system to resolubilize and reactivate stress-denatured proteins. In yeast this machinery also promotes propagation of prions by fragmenting prion polymers. We previously showed the bacterial Hsp100 machinery cooperates with the yeast Hsp40 Ydj1 to support yeast thermotolerance and with the yeast Hsp40 Sis1 to propagate [PSI+] prions. Here we find these Hsp40s similarly directed specific activities of the yeast Hsp104-based machinery. By assessing the ability of Ydj1-Sis1 hybrid proteins to complement Ydj1 and Sis1 functions we show their C-terminal substrate-binding domains determined distinctions in these and other cellular functions of Ydj1 and Sis1. We find propagation of [URE3] prions was acutely sensitive to alterations in Sis1 activity, while that of [PIN+] prions was less sensitive than [URE3], but more sensitive than [PSI+]. These findings support the ideas that overexpressing Ydj1 cures [URE3] by competing with Sis1 for interaction with the Hsp104-based disaggregation machine, and that different prions rely differently on activity of this machinery, which can explain the various ways they respond to alterations in chaperone function.

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Known prions (infectious proteins) are self-propagating amyloids or conformationally altered proteins, but in theory an enzyme necessary for its own activation could also be a prion (or a gene composed of protein). We show that yeast protease B is such a prion, called [beta].[beta] is infectious, reversibly curable, and its de novo generation is induced by overexpression of the pro-protease. Present in normal cells but masked by the functionally redundant protease A, [beta] is advantageous during starvation and necessary for sporulation. We propose that other enzymes whose active, modified, form is necessary for their maturation might also be prions.

Using randomized stimulus onset asynchrony (SOAs), the authors traced the time course of Stroop interference and facilitation in normal participants and participants with schizophrenia. Unlike earlier findings using blocked SOAs, singular peaks in interference, facilitation, or both occurred at particular SOAs. The peaks of normal participants and participants with schizophrenia differed. Findings are congruent with a model of Stroop performance that posits individual differences in processing speeds of target and nontarget stimulus dimensions, coupled with critical points in response selection. Participants with schizophrenia also showed more overall interference than normal control participants. A second experiment that added a temporal gap between the distractor word and target color obliterated Stroop effects only for individuals with schizophrenia. These findings provide a new empirical basis for models of Stroop effects. They are also consistent with hypotheses about the importance of the prefrontal cortex for working memory and prefrontal dysfunction in schizophrenia.