Hydrologic Data for Urban Studies in The Austin, Texas, Metropolitan Area, 1982

The technical report mentions Waller Creek as a main stream in the study area, but a preliminary search provides no results to specific data from the site.Hydrologic investigations of urban watersheds in Texas were begun by the U.S. Geological Survey in 1954. Studies are now in progress in Austin, and Houston. Studies have been completed in the Dallas, Fort Worth, and San Antonio areas. The Geological Survey, in cooperation with the Texas Department of Water Resources, began hydrologic studies in the Austin urban area in 1954. In cooperation with the city of Austin, the program was expanded in 1975 to include additional streamflow and rainfall gaging stations, and the collection of surface water-quality data. In 1978, the program was expanded to include a ground-water resources study of the South Austin metropolitan area in the Balcones Fault Zone.Waller Creek Working Grou

The SPOC proteins DIDO3 and PHF3 co-regulate gene expression and neuronal differentiation

Transcription is regulated by a multitude of activators and repressors, which bind to the RNA polymerase II (Pol II) machinery and modulate its progression. Death-inducer obliterator 3 (DIDO3) and PHD finger protein 3 (PHF3) are paralogue proteins that regulate transcription elongation by docking onto phosphorylated serine-2 in the C-terminal domain (CTD) of Pol II through their SPOC domains. Here, we show that DIDO3 and PHF3 form a complex that bridges the Pol II elongation machinery with chromatin and RNA processing factors and tethers Pol II in a phase-separated microenvironment. Their SPOC domains and C-terminal intrinsically disordered regions are critical for transcription regulation. PHF3 and DIDO exert cooperative and antagonistic effects on the expression of neuronal genes and are both essential for neuronal differentiation. In the absence of PHF3, DIDO3 is upregulated as a compensatory mechanism. In addition to shared gene targets, DIDO specifically regulates genes required for lipid metabolism. Collectively, our work reveals multiple layers of gene expression regulation by the DIDO3 and PHF3 paralogues, which have specific, co-regulatory and redundant functions in transcription

The SPOC domain is a phosphoserine binding module that bridges transcription machinery with co- and post-transcriptional regulators

The heptad repeats of the C-terminal domain (CTD) of RNA polymerase II (Pol II) are extensively modified throughout the transcription cycle. The CTD coordinates RNA synthesis and processing by recruiting transcription regulators as well as RNA capping, splicing and 3'end processing factors. The SPOC domain of PHF3 was recently identified as a CTD reader domain specifically binding to phosphorylated serine-2 residues in adjacent CTD repeats. Here, we establish the SPOC domains of the human proteins DIDO, SHARP (also known as SPEN) and RBM15 as phosphoserine binding modules that can act as CTD readers but also recognize other phosphorylated binding partners. We report the crystal structure of SHARP SPOC in complex with CTD and identify the molecular determinants for its specific binding to phosphorylated serine-5. PHF3 and DIDO SPOC domains preferentially interact with the Pol II elongation complex, while RBM15 and SHARP SPOC domains engage with writers and readers of mA, the most abundant RNA modification. RBM15 positively regulates mA levels and mRNA stability in a SPOC-dependent manner, while SHARP SPOC is essential for its localization to inactive X-chromosomes. Our findings suggest that the SPOC domain is a major interface between the transcription machinery and regulators of transcription and co-transcriptional processes

PHF3 regulates neuronal gene expression through the Pol II CTD reader domain SPOC

The C-terminal domain (CTD) of the largest subunit of RNA polymerase II (Pol II) is a regulatory hub for transcription and RNA processing. Here, we identify PHD-finger protein 3 (PHF3) as a regulator of transcription and mRNA stability that docks onto Pol II CTD through its SPOC domain. We characterize SPOC as a CTD reader domain that preferentially binds two phosphorylated Serine-2 marks in adjacent CTD repeats. PHF3 drives liquid-liquid phase separation of phosphorylated Pol II, colocalizes with Pol II clusters and tracks with Pol II across the length of genes. PHF3 knock-out or SPOC deletion in human cells results in increased Pol II stalling, reduced elongation rate and an increase in mRNA stability, with marked derepression of neuronal genes. Key neuronal genes are aberrantly expressed in Phf3 knock-out mouse embryonic stem cells, resulting in impaired neuronal differentiation. Our data suggest that PHF3 acts as a prominent effector of neuronal gene regulation by bridging transcription with mRNA decay

The nature and impacts of fines in smelter-grade alumina

Fines in smelter-grade aluminas art recognized (is a significant process problem in aluminum smelting. However understanding the nature of this fine material and how it impacts the reduction process arc, less clearly understood The combination of new analytical methods such as variable pressure scanning electron microscopy and very; high field solid state nuclear magnetic resonance provide new insights into the phases present and their spatial distribution within aluminas, and suggest how such fine materials are generated, particularly during calcination in the alumina refinery