FRANKLIN COUNTY, IOWA'S PROGRAM IN PUBLIC AFFAIRS

Public Economics,

Permanent Draft Genome sequence for Frankia sp. strain CcI49, a Nitrogen-Fixing Bacterium Isolated from Casuarina cunninghamiana that Infects Elaeagnaceae

Frankia sp. strain CcI49 was isolated from Casuarina cunninghamiana nodules. However the strain was unable to re-infect Casuarina, but was able to infect other actinorhizal plants including Elaeagnaceae. Here, we report the 9.8-Mbp draft genome sequence of Frankia sp. strain CcI49 with a G+C content of 70.5 % and 7,441 candidate protein-encoding genes. Analysis of the genome revealed the presence of a bph operon involved in the degradation of biphenyls and polychlorinated biphenyls

Altered dynamic postural control during gait termination following concussion

Impaired postural control is a cardinal symptom following concussion. Planned gait termination (GT) is a non-novel, dynamic task that challenges postural control in individuals with neurological deficits, and it could be an impactful measure for identifying dynamic postural control impairments following concussion. Therefore, the purpose of this study was to assess acute post-concussion dynamic postural control utilizing a planned GT task. The concussion participants (n= 19, age: 19.0 ± 0.8 years, height: 177.0 ± 10.1 cm, weight: 83.3 ± 20.0 kg) completed five planned GT trials during preseason baseline testing (Baseline) and on Day 1 post-concussion (Day-1). Healthy control participants (n=19, age: 20.4 ± 1.2 years, height: 173.8 ± 8.9 cm, weight: 80.2 ± 17.6 kg) completed the same trials a week apart. The dependent variables of interest included COP displacement and velocity in the mediolateral (ML) and anteroposterior (AP) axes during the three phases (braking, transitional, stabilization) of planned GT. There were significant interactions observed in both the braking ML and transitional AP displacement (p= 0.042, p= 0.030) and velocity (p= 0.027, p= 0.030). These results suggest a conservative post-concussion motor control strategy during planned GT. Further, these results support the use of dynamic postural control tasks as measures of post-concussion impairments

Combinatorial control of temporal gene expression in the Drosophila wing by enhancers and core promoters

Abstract Background The transformation of a developing epithelium into an adult structure is a complex process, which often involves coordinated changes in cell proliferation, metabolism, adhesion, and shape. To identify genetic mechanisms that control epithelial differentiation, we analyzed the temporal patterns of gene expression during metamorphosis of the Drosophila wing. Results We found that a striking number of genes, approximately 50% of the Drosophila transcriptome, exhibited changes in expression during a time course of wing development. While cis-acting enhancer sequences clearly correlated with these changes, a stronger correlation was discovered between core-promoter types and the dynamic patterns of gene expression within this differentiating tissue. In support of the hypothesis that core-promoter type influences the dynamics of expression, expression levels of several TATA-box binding protein associated factors (TAFs) and other core promoter-associated components changed during this developmental time course, and a testes-specific TAF (tTAF) played a critical role in timing cellular differentiation within the wing. Conclusions Our results suggest that the combinatorial control of gene expression via cis-acting enhancer sequences and core-promoter types, determine the complex changes in gene expression that drive morphogenesis and terminal differentiation of the Drosophila wing epithelium.http://deepblue.lib.umich.edu/bitstream/2027.42/112935/1/12864_2012_Article_4965.pd

Skeletal Deficits in Male and Female down Syndrome Model Mice Arise Independent of Normalized Dyrk1a Expression in Osteoblasts

Trisomy 21 (Ts21) causes alterations in skeletal development resulting in decreased bone mass, shortened stature and weaker bones in individuals with Down syndrome (DS). There is a sexual dimorphism in bone mineral density (BMD) deficits associated with DS with males displaying earlier deficits than females. The relationships between causative trisomic genes, cellular mechanisms, and influence of sex in DS skeletal abnormalities remain unknown. One hypothesis is that the low bone turnover phenotype observed in DS results from attenuated osteoblast function, contributing to impaired trabecular architecture, altered cortical geometry, and decreased mineralization. DYRK1A, found in three copies in humans with DS, Ts65Dn, and Dp1Tyb DS model mice, has been implicated in the development of postnatal skeletal phenotypes associated with DS. Reduced copy number of Dyrk1a to euploid levels from conception in an otherwise trisomic Ts65Dn mice resulted in a rescue of appendicular bone deficits, suggesting DYRK1A contributes to skeletal development and homeostasis. We hypothesized that reduction of Dyrk1a copy number in trisomic osteoblasts would improve cellular function and resultant skeletal structural anomalies in trisomic mice. Female mice with a floxed Dyrk1a gene (Ts65Dn,Dyrk1afl/wt) were mated with male Osx-Cre+ (expressed in osteoblasts beginning around E13.5) mice, resulting in reduced Dyrk1a copy number in mature osteoblasts in Ts65Dn,Dyrk1a+/+/Osx-Cre P42 male and female trisomic and euploid mice, compared with littermate controls. Male and female Ts65Dn,Dyrk1a+/+/+ (3 copies of DYRK1A in osteoblasts) and Ts65Dn,Dyrk1a+/+/Osx-Cre (2 copies of Dyrk1a in osteoblasts) displayed similar defects in both trabecular architecture and cortical geometry, with no improvements with reduced Dyrk1a in osteoblasts. This suggests that trisomic DYRK1A does not affect osteoblast function in a cell-autonomous manner at or before P42. Although male Dp1Tyb and Ts65Dn mice exhibit similar skeletal deficits at P42 in both trabecular and cortical bone compartments between euploid and trisomic mice, female Ts65Dn mice exhibit significant cortical and trabecular deficits at P42, in contrast to an absence of genotype effect in female Dp1Tyb mice in trabecular bone. Taken together, these data suggest skeletal deficits in DS mouse models and are sex and age dependent, and influenced by strain effects, but are not solely caused by the overexpression of Dyrk1a in osteoblasts. Identifying molecular and cellular mechanisms, disrupted by gene dosage imbalance, that are involved in the development of skeletal phenotypes associated with DS could help to design therapies to rescue skeletal deficiencies seen in DS