Solar wind protons at 1 AU: trends and bounds, constraints and correlations

The proton temperature anisotropy in the solar wind exhibits apparent bounds which are compatible with the theoretical constraints imposed by temperature-anisotropy driven kinetic instabilities. Recent statistical analyses based on conditional averaging indicate that near these theoretical constraints the solar wind protons have typically enhanced temperatures and a weaker collisionality. Here we carefully analyze the solar wind data and show that these results are a consequence of superposition of multiple correlations in the solar wind, namely, they mostly result from the correlation between the proton temperature and the solar wind velocity and from the superimposed anti-correlation between the proton temperature anisotropy and the proton parallel beta in the fast solar wind. Colder and more collisional data are distributed around temperature isotropy whereas hotter and less collisional data have a wider range of the temperature anisotropy anti-correlated with the proton parallel beta with signatures of constraints owing to the temperature-anisotropy driven instabilities. However, most of the hot and weakly collisional data, including the hottest and least collisional ones, lies far from the marginal stability regions. Consequently, we conclude that there is no clear relation between the enhanced temperatures and instability constraints and that the conditional averaging used for these analyses must be used carefully and need to be well tested.Comment: Accepted for publication in ApJ

Overproduction of PDR3 Suppresses Mitochondrial Import Defects Associated with a TOM70 Null Mutation by Increasing the Expression of TOM72 in Saccharomyces cerevisiae

Most mitochondrial proteins are synthesized with cleavable amino-terminal targeting signals that interact with the mitochondrial import machinery to facilitate their import from the cytosol. We previously reported that the presequence of the F1-ATPase beta subunit precursor (pre-F1beta ) acts as an intramolecular chaperone that maintains the precursor in an import-competent conformation prior to import (P. Hajek, J. Y. Koh, L. Jones, and D. M. Bedwell, Mol. Cell. Biol. 17:7169-7177, 1997). We also found that a mutant form of pre-F1beta with a minimal targeting signal (Delta 1,2 pre-F1beta) is inefficiently imported into mitochondria because it rapidly folds into an import-incompetent conformation. We have now analyzed the consequences of reducing the pre-F1beta targeting signal to a minimal unit in more detail. We found that Delta 1,2 pre-F1beta is more dependent upon the Tom70p receptor for import than WT pre-F1beta is, resulting in a growth defect on a nonfermentable carbon source at 15°C. Experiments using an in vitro mitochondrial protein import system suggest that Tom70p functions to maintain a precursor containing the Delta 1,2 pre-F1beta import signal in an import-competent conformation. We also identified PDR3, a transcriptional regulator of the pleiotropic drug resistance network, as a multicopy suppressor of the mitochondrial import defects associated with Delta 1,2 pre-F1beta in a tom70Delta strain. The overproduction of PDR3 mediated this effect by increasing the import of Delta 1,2 pre-F1beta into mitochondria. This increased the mitochondrial ATP synthase activity to the extent that growth of the mutant strain was restored under the selective conditions. Analysis of the transcription patterns of components of the mitochondrial outer membrane import machinery demonstrated that PDR3 overproduction increased the expression of TOM72, a little studied TOM70 homologue. These results suggest that Tom72p possesses overlapping functions with Tom70p and that the pleiotropic drug resistance network plays a previously unappreciated role in mitochondrial biogenesis