ALBERT

Description: Deformed lunar zircons yielding U-Pb ages from 4333 Ma to 1407 Ma have been interpreted as dating discrete impacts on the Moon. However, the cause of age resetting in lunar zircons is equivocal; as ex situ grains in breccias, they lack lithologic context and most do not contain microstructures diagnostic of shock that are found in terrestrial zircons. Detrital shocked zircons provide a terrestrial analog to ex situ lunar grains, for both identifying diagnostic shock evidence and also evaluating the feasibility of dating impacts with ex situ zircons. Electron backscatter diffraction and sensitive high-resolution ion microprobe U-Pb analysis of zircons eroded from the ca. 2020 Ma Vredefort impact structure (South Africa) show that complete impact-age resetting did not occur in microstructural domains characterized by microtwins, planar fractures, and low-angle boundaries, which record ages from 2890 Ma to 2645 Ma. An impact age of 1975 ± 39 Ma was detected in neoblasts within a granular zircon that also contains shock microtwins, which link neoblast formation to the impact. However, we show that granular texture can form during regional metamorphism, and thus is not unique to impact environments. These results demonstrate that dating an impact with ex situ shocked zircon requires identifying diagnostic shock evidence to establish impact provenance, and then targeting specific age-reset microstructures. With the recognition that zircon can deform plastically in both impact and magmatic environments, age-resetting in lunar zircons that lack diagnostic shock deformation may record magmatic processes rather than discrete impacts. Identifying shock microstructures that record complete age resetting for geochronological analysis is thus crucial for constructing accurate zircon-based impact chronologies for the Moon, Earth, or other planetary bodies.

Description: 〈p〉Phosphoregulation, in which the addition of a negatively charged phosphate group modulates protein activity, enables dynamic cellular responses. To understand how new phosphoregulation might be acquired, we mutationally scanned the surface of a prototypical yeast kinase (Kss1) to identify potential regulatory sites. The data revealed a set of spatially distributed "hotspots" that might have coevolved with the active site and preferentially modulated kinase activity. By engineering simple consensus phosphorylation sites at these hotspots, we rewired cell signaling in yeast. Using the same approach with a homolog yeast mitogen-activated protein kinase, Hog1, we introduced new phosphoregulation that modified its localization and signaling dynamics. Beyond revealing potential use in synthetic biology, our findings suggest that the identified hotspots contribute to the diversity of natural allosteric regulatory mechanisms in the eukaryotic kinome and, given that some are mutated in cancers, understanding these hotspots may have clinical relevance to human disease.〈/p〉