The effects of urbanization on floods in the Austin metropolitan area, Texas

This report looks at compiled data from 1956-1980 to "provide a technique for estimating the magnitude and frequency of flood-peak discharges at ungaged sites and to estimate the effects of changes in urbanization on flood peaks."The effects of urbanization on flood peaks in streams in the Austin metropolitan area were studied in two separate analyses. In the first analysis, annual peak discharge records at 13 streamflow-gaging sites were used to compute a recorded flood frequency relation for each site. Rainfall and streamflow data for 10 to 20 storms for each of these sites were used to calibrate a rainfall-runoff model in which a 55-year rainfall record was used to simulate 55 annual peak discharges. These simulated discharges also were used to develop a flood-frequency relation at each site. The flood-frequency relations from recorded and generated data were then combined by weighting the recorded flood frequency by the years of record at each site to produce a combined (or weighted) flood frequency at each site. Flood frequencies for all 13 sites were subsequently regressed against basin characteristics at each site to determine possible effects of urbanization. The regression analysis of the combined flood-frequency data for the 13 sites yielded an equation for estimating floods of a given recurrence interval at ungaged sites in the Austin area as a function of the contributing drainage area, the total impervious area percentage, and basin shape. The regression equation estimates that a near fully developed hypothetical drainage basin (impervious area percentage, 45) would have discharges for the 2- and 100-year recurrence interval that are 99 percent and 73 percent greater, respectively, than discharges for those frequencies from a rural drainage basin (impervious percentage, 0). In the second analysis, records at one streamflow-gaging site on Waller Creek were analyzed for changes in rainfall-runoff and flood-frequency relations due to urbanization. Annual peak discharges from 1956 to 1980 and data from a total of 80 storms at the Waller Creek site were analyzed. Both analyses showed increases comparable to those predicted using the equations developed from the 13-station analysis. The last 14 years of record (the near fully developed land-use stage for the Waller Creek analysis) at the two sites on Waller Creek were part of the 13-station analysis. The U.S. Geological Survey, in cooperation with the Texas Department of Water Resources began limited investigations of urban watersheds in Austin in 1954, with the installation of two streamflow-gaging stations and three recording rain gages in the Waller Creek watershed. In 1963, a streamflow gage and three recording rain gages were installed at Wilbarger Creek watershed, a rural area just north of Austin. In cooperation with the City of Austin, the urban study was expanded in 1975 to include additional streamflow and rainfall gaging stations and the collection of surface water-quality data. The number of streamflow-gaging stations increased from 2 to 25 and the number of recording rain gages increased from 3 to 31.Waller Creek Working Grou

Location of catalase in crystalline peroxisomes of methanol-grown Hansenula polymorpha

We have studied the intraperoxisomal location of catalase in peroxisomes of methanol-grown Hansenula polymorpha by (immuno)cytochemical means. In completely crystalline peroxisomes, in which the crystalline matrix is composed of octameric alcohol oxidase (AO) molecules, most of the catalase protein is located in a narrow zone between the crystalloid and the peroxisomal membrane. In non-crystalline organelles the enzyme was present throughout the peroxisomal matrix. Other peroxisomal matrix enzymes studied for comparison, namely dihydroxyacetone synthase, amine oxidase and malate synthase, all were present throughout the AO crystalloid. The advantage of location of catalase at the edges of the AO crystalloids for growth of the organism on methanol is discussed.

Fostering Autonomous Learning in University Language Students: Best Teaching Practices to Encourage Life-Long Learning

Veenhuis, S. J. Fostering Autonomous Learning in University Language Students: Best Teaching Practices to Encourage Life-Long Learning. (2020) Fostering autonomous language learning in university students is advantageous to their ability to push their language learning further. Implementation, however, is not a simple practice. There are many roles the teacher, students, and university must play. This capstone uses relevant literature to answer the research question, how can teachers of English as a foreign language at the university level help their students become successful, autonomous learners? The project informed by this capstone outlines a professional development training to help teachers understand how to implement autonomous learning in their classrooms by helping their students identify their strengths and weaknesses in the language, set achievable goals, and create a study plan that will help students to reach their individual goals outside of the classroom using teacher recommended learning strategies and resources. A major limitation of this capstone is a lack of opportunities for English foreign language (EFL) teachers to attend long-term professional development trainings. A possible implication of this project is that a conversation needs to be started about providing more training opportunities to EFL professionals and addressing the subject of autonomous learning in teacher training programs

Pay32p of the Yeast Yarrowia lipolytica Is an Intraperoxisomal Component of the Matrix Protein Translocation Machinery

Pay mutants of the yeast Yarrowia lipolytica fail to assemble functional peroxisomes. One mutant strain, pay32-1, has abnormally small peroxisomes that are often found in clusters surrounded by membranous material. The functionally complementing gene PAY32 encodes a protein, Pay32p, of 598 amino acids (66,733 D) that is a member of the tetratricopeptide repeat family. Pay32p is intraperoxisomal. In wild-type peroxisomes, Pay32p is associated primarily with the inner surface of the peroxisomal membrane, but ~30% of Pay32p is localized to the peroxisomal matrix. The majority of Pay32p in the matrix is complexed with two polypeptides of 62 and 64 kD recognized by antibodies to SKL (peroxisomal targeting signal-1). In contrast, in peroxisomes of the pay32-1 mutant, Pay32p is localized exclusively to the matrix and forms no complex. Biochemical characterization of the mutants pay32-1 and pay32-KO (a PAY32 gene disruption strain) showed that Pay32p is a component of the peroxisomal translocation machinery. Mutations in the PAY32 gene prevent the translocation of most peroxisome-bound proteins into the peroxisomal matrix. These proteins, including the 62-kD anti-SKL-reactive polypeptide, are trapped in the peroxisomal membrane at an intermediate stage of translocation in pay32 mutants. Our results suggest that there are at least two distinct translocation machineries involved in the import of proteins into peroxisomes.

A comparative study of peroxisomal structures in Hansenula polymorpha pex mutants

In a recent study, we performed a systematic genome analysis for the conservation of genes involved in peroxisome biogenesis (PEX genes) in various fungi. We have now performed a systematic study of the morphology of peroxisome remnants (‘ghosts’) in Hansenula polymorpha pex mutants (pex1–pex20) and the level of peroxins and matrix proteins in these strains. To this end, all available H. polymorpha pex strains were grown under identical cultivation conditions in glucose-limited chemostat cultures and analyzed in detail. The H. polymorpha pex mutants could be categorized into four distinct groups, namely pex mutants containing: (1) virtually normal peroxisomal structures (pex7, pex17, pex20); (2) small peroxisomal membrane structures with a distinct lumen (pex2, pex4, pex5, pex10, pex12, pex14); (3) multilayered membrane structures lacking apparent matrix protein content (pex1, pex6, pex8, pex13); and (4) no peroxisomal structures (pex3, pex19).

The Hansenula polymorpha PER8 Gene Encodes a Novel Peroxisomal Integral Membrane Protein Involved in Proliferation

We previously described the isolation of mutants of the methylotrophic yeast Hansenula polymorpha that are defective in peroxisome biogenesis. Here, we describe the characterization of one of these mutants, per8, and the cloning of the PER8 gene. In either methanol or methylamine medium, conditions that normally induce the organdies, per8 cells contain no peroxisome-like structures and peroxisomal enzymes are located in the cytosol. The sequence of PER8 predicts that its product (Per8p) is a novel polypeptide of 34 kD, and antibodies against Per8p recognize a protein of 31 kD. Analysis of the primary sequence of Per8p revealed a 39-amino-acid cysteine-rich segment with similarity to the C3HC4 family of zinc-finger motifs. Overexpression of PER8 results in a markedly enhanced increase in peroxisome numbers. We show that Per8p is an integral membrane protein of the peroxisome and that it is concentrated in the membranes of newly formed organdies. We propose that Per8p is a component of the molecular machinery that controls the proliferation of this organelle.

Hansenula polymorpha: An attractive model organism for molecular studies of peroxisome biogenesis and function

In wild-type Hansenula polymorpha the proliferation of peroxisomes is induced by various unconventional carbon- and nitrogen sources. Highest induction levels, up to 80% of the cytoplasmic volume, are observed in cells grown in methanol-limited chemostat cultures. Based on our accumulated experience, we are now able to precisely adjust both the level of peroxisome induction as well as their protein composition by specific adaptations in growth conditions. During the last few years a series of peroxisome-deficient (per) mutants of H. polymorpha have been isolated and characterized. Phenotypically these mutants are characterized by the fact that they are not able to grow on methanol. Three mutant phenotypes were defined on the basis of morphological criteria, namely: (a) mutants completely lacking peroxisomes (Per-; 13 complementation groups); (b) mutants containing few small peroxisomes which are partly impaired in the peroxisomal import of matrix proteins (Pim-; five complementation groups); and (c) mutants with aberrations in the peroxisomal substructure (Pss-; two complementation groups). In addition, several conditional Per-, Pim- and Pss- mutants have been obtained. In all cases the mutant phenotype was shown to be caused by a recessive mutation in one gene. However, we observed that different mutations in one gene may cause different morphological mutant phenotypes. A detailed genetic analysis revealed that several PER genes, essential for peroxisome biogenesis, are tightly linked and organized in a hierarchical fashion. The use of both constitual and conditional per mutants in current and future studies of the molecular mechanisms controlling peroxisome biogenesis and function is discussed.