General Microbiology (Dalton State)

This Grants Collection for General Microbiology was created under a Round Nine ALG Textbook Transformation Grant. Affordable Learning Georgia Grants Collections are intended to provide faculty with the frameworks to quickly implement or revise the same materials as a Textbook Transformation Grants team, along with the aims and lessons learned from project teams during the implementation process. Documents are in .pdf format, with a separate .docx (Word) version available for download. Each collection contains the following materials: Linked Syllabus Initial Proposal Final Reporthttps://oer.galileo.usg.edu/biology-collections/1021/thumbnail.jp

Deficiency of Complement Component C1Q Prevents Cerebrovascular Damage and White Matter Loss in a Mouse Model of Chronic Obesity.

Age-related cognitive decline and many dementias involve complex interactions of both genetic and environmental risk factors. Recent evidence has demonstrated a strong association of obesity with the development of dementia. Furthermore, white matter damage is found in obese subjects and mouse models of obesity. Here, we found that components of the complement cascade, including complement component 1qa (C1QA) and C3 are increased in the brain of Western diet (WD)-fed obese mice, particularly in white matter regions. To functionally test the role of the complement cascade in obesity-induced brain pathology, female and male mice deficient in C1QA, an essential molecule in the activation of the classical pathway of the complement cascade, were fed a WD and compared with WD-fed wild type (WT) mice, and t

Transcriptional profiling predicts running promotes cerebrovascular remodeling in young but not midlife mice.

BACKGROUND: The incidence of dementia and cognitive decline is increasing with no therapy or cure. One of the reasons treatment remains elusive is because there are various pathologies that contribute to age-related cognitive decline. Specifically, with Alzheimer\u27s disease, targeting to reduce amyloid beta plaques and phosphorylated tau aggregates in clinical trials has not yielded results to slow symptomology, suggesting a new approach is needed. Interestingly, exercise has been proposed as a potential therapeutic intervention to improve brain health and reduce the risk for dementia, however the benefits throughout aging are not well understood. RESULTS: To better understand the effects of exercise, we preformed transcriptional profiling on young (1-2 months) and midlife (12 months) C57BL/6 J (B6) male mice after 12 weeks of voluntary running. Data was compared to age-matched sedentary controls. Interestingly, the midlife running group naturally broke into two cohorts based on distance ran - either running a lot and more intensely (high runners) or running less and less intensely (low runners). Midlife high runners had lower LDL cholesterol as well as lower adiposity (%fat) compared to sedentary, than midlife low runners compared to sedentary suggesting more intense running lowered systemic markers of risk for age-related diseases including dementias. Differential gene analysis of transcriptional profiles generated from the cortex and hippocampus showed thousands of differentially expressed (DE) genes when comparing young runners to sedentary controls. However, only a few hundred genes were DE comparing either midlife high runners or midlife low runners to midlife sedentary controls. This indicates that, in our study, the effects of running are reduced through aging. Gene set enrichment analyses identified enrichment of genes involved in extracellular matrix (ECM), vascular remodeling and angiogenesis in young runners but not midlife runners. These genes are known to be expressed in multiple vascular-related cell types including astrocytes, endothelial cells, pericytes and smooth muscle cells. CONCLUSIONS: Taken together these results suggest running may best serve as a preventative measure to reduce risk for cerebrovascular decline. Ultimately, this work shows that exercise may be more effective to prevent dementia if introduced at younger ages

Clustering of transcriptional profiles identifies changes to insulin signaling as an early event in a mouse model of Alzheimer’s disease

BACKGROUND: Alzheimer’s disease affects more than 35 million people worldwide but there is no known cure. Age is the strongest risk factor for Alzheimer’s disease but it is not clear how age-related changes impact the disease. Here, we used a mouse model of Alzheimer’s disease to identify age-specific changes that occur prior to and at the onset of traditional Alzheimer-related phenotypes including amyloid plaque formation. To identify these early events we used transcriptional profiling of mouse brains combined with computational approaches including singular value decomposition and hierarchical clustering. RESULTS: Our study identifies three key events in early stages of Alzheimer’s disease. First, the most important drivers of Alzheimer’s disease onset in these mice are age-specific changes. These include perturbations of the ribosome and oxidative phosphorylation pathways. Second, the earliest detectable disease-specific changes occur to genes commonly associated with the hypothalamic-adrenal-pituitary (HPA) axis. These include the down-regulation of genes relating to metabolism, depression and appetite. Finally, insulin signaling, in particular the down-regulation of the insulin receptor substrate 4 (Irs4) gene, may be an important event in the transition from age-related changes to Alzheimer’s disease specific-changes. CONCLUSION: A combination of transcriptional profiling combined with computational analyses has uncovered novel features relevant to Alzheimer’s disease in a widely used mouse model and offers avenues for further exploration into early stages of AD

Genetic perturbations of disease risk genes in mice capture transcriptomic signatures of late-onset Alzheimer\u27s disease.

BACKGROUND: New genetic and genomic resources have identified multiple genetic risk factors for late-onset Alzheimer\u27s disease (LOAD) and characterized this common dementia at the molecular level. Experimental studies in model organisms can validate these associations and elucidate the links between specific genetic factors and transcriptomic signatures. Animal models based on LOAD-associated genes can potentially connect common genetic variation with LOAD transcriptomes, thereby providing novel insights into basic biological mechanisms underlying the disease. METHODS: We performed RNA-Seq on whole brain samples from a panel of six-month-old female mice, each carrying one of the following mutations: homozygous deletions of Apoe and Clu; hemizygous deletions of Bin1 and Cd2ap; and a transgenic APOEε4. Similar data from a transgenic APP/PS1 model was included for comparison to early-onset variant effects. Weighted gene co-expression network analysis (WGCNA) was used to identify modules of correlated genes and each module was tested for differential expression by strain. We then compared mouse modules with human postmortem brain modules from the Accelerating Medicine\u27s Partnership for AD (AMP-AD) to determine the LOAD-related processes affected by each genetic risk factor. RESULTS: Mouse modules were significantly enriched in multiple AD-related processes, including immune response, inflammation, lipid processing, endocytosis, and synaptic cell function. WGCNA modules were significantly associated with Apoe CONCLUSIONS: This study of genetic mouse models provides a basis to dissect the role of AD risk genes in relevant AD pathologies. We determined that different genetic perturbations affect different molecular mechanisms comprising AD, and mapped specific effects to each risk gene. Our approach provides a platform for further exploration into the causes and progression of AD by assessing animal models at different ages and/or with different combinations of LOAD risk variants

Transcriptome profiling of brain myeloid cells revealed activation of Itgal, Trem1, and Spp1 in western diet-induced obesity.

BACKGROUND: Environmental factors are critical in the development of age-related cognitive decline and dementia. A western diet (WD) can cause nutrient deficiency and inflammation that could impact cognition directly. It is increasingly recognized that innate immune responses by brain myeloid cells, such as resident microglia, and infiltrating peripheral monocytes/macrophages may represent an essential link between a WD, cognitive decline, and dementia. Our previous data demonstrated that chronic consumption of a WD induced inflammation through brain myeloid cells in aging mice and a mouse model of Alzheimer\u27s disease (AD). However, the subtypes of myeloid cells that contribute to the WD-induced inflammation remain unclear. METHODS: C57BL/6J (B6), myeloid cell reporter mice (B6.Ccr2 RESULTS: Ccr2::RFP expressing myeloid cells were significantly increased in brains of WD- compared to CD-fed mice, but were not elevated in Ccr2-deficient WD-fed mice. The percent of CD11b+CD45 CONCLUSIONS: These data further support the model that peripheral myeloid cells enter the brain in response to diet-induced obesity. Elucidating their contribution to age-related cognitive decline and age-related neurodegenerative diseases should offer new avenues for therapeutic intervention in Alzheimer\u27s disease and related dementias, where diet/obesity are major risk factors

2002 Grape Cultivar Trial Performance in 2009

To identify grape cultivars adapted to Iowa, a cultivar by management system trial was established in 2002 at the Iowa State University (ISU) Horticulture Research Station (HRS) and the ISU Armstrong Research Farm (ARF) with a grant from the Leopold Center of Sustainable Agriculture. Fifteen cultivars, including ten wine and five seedless table cultivars, were being evaluated under three management systems that were discontinued in 2008. This report summarizes the cultivar performance for the 2009 growing season

Brood parasitism and nest survival of Brown-headed Cowbird hosts at high-elevation riparian sites in the eastern Sierra Nevada, California

Deciduous riparian ecosystems in the western United States provide habitat for a higher density of breeding birds than reported for any other avian habitat type and provide habitat for more breeding bird species than adjacent uplands. On the east slope of the Sierra Nevada, riparian ecosystems make up \u3c1% of United States Forest Service lands yet experience a disproportionate amount of recreational use and development. Two of these developments, pack-station corrals and campgrounds, provide foraging opportunities for the Brown-headed Cowbird (Molothrus ater)—an obligate brood parasite that forages on bare ground and feedlots but typically commutes to distinct shrubland or woodland habitats for breeding. We examined nest survival, brood parasitism, breeding phenology, and causes of nest failure for birds at North Lake and Rock Creek: 2 high-elevation (\u3e2500 m) riparian breeding habitats adjacent to recreational development and within cowbird commuting distance to additional potential foraging sites. Nest survival tended to be higher for host species at Rock Creek than for those at North Lake, but parasitism rates were not significantly different between plots. Of 21 open-cup nesting species, 12 were parasitized. We found the highest rate of parasitism (92%) for Warbling Vireos (Vireo gilvus) at North Lake, and parasitism contributed to lower total nest survival there (14%). For nearly all species, parasitized nests were less successful and produced fewer young than nonparasitized nests. However, predation was the leading cause of complete nest failure across all species and contributed to the lowest total nest survival estimates for Western Wood-Pewees (Contopus sordidulus, 11%) and Dusky Flycatchers (Empidonax oberholseri, 15%) at North Lake and for Dark-eyed Juncos (Junco hyemalis, 15%) at Rock Creek. Nest survival was relatively high for Western Wood-Pewees (41%) at Rock Creek and for Yellow Warblers (Dendroica petechia, 47%) at North Lake. We noted whether the arrival of pack animals at pack-station corrals contributed to variation in cowbird numbers at corrals or in parasitism rates at the 2 sites. Cowbirds occupied corrals before and after pack-stock arrival, and most host clutches were completed prior to pack-stock arrival at nearby corrals, suggesting that the presence of pack animals did not directly affect cowbird host species

2002 Grape Cultivar Trial Performance

To identify grape cultivars adapted to Iowa, a cultivar by management system trial was established in 2002 at the Iowa State University (ISU) Horticulture Research Station (HRS) and the ISU Armstrong Research Farm (ARF) with a grant from the Leopold Center of Sustainable Agriculture. Fifteen cultivars, including ten wine and five seedless table cultivars, were being evaluated under three management systems that were discontinued in 2008. This report summarizes the cultivar performance for the 2010 growing season