Functionality of the GAL4/UAS system in Tribolium requires the use of endogenous core promoters

<p>Abstract</p> <p>Background</p> <p>The red flour beetle <it>Tribolium castaneum </it>has developed into an insect model system second only to <it>Drosophila</it>. Moreover, as a coleopteran it represents the most species-rich metazoan taxon which also includes many pest species. The genetic toolbox for <it>Tribolium </it>research has expanded in the past years but spatio-temporally controlled misexpression of genes has not been possible so far.</p> <p>Results</p> <p>Here we report the establishment of the GAL4/UAS binary expression system in <it>Tribolium castaneum</it>. Both GAL4Δ and GAL4VP16 driven by the endogenous heat shock inducible promoter of the <it>Tribolium hsp68 </it>gene are efficient in activating reporter gene expression under the control of the Upstream Activating Sequence (UAS). UAS driven ubiquitous tGFP fluorescence was observed in embryos within four hours after activation while <it>in-situ </it>hybridization against tGFP revealed expression already after two hours. The response is quick in relation to the duration of embryonic development in <it>Tribolium </it>- 72 hours with segmentation being completed after 24 hours - which makes the study of early embryonic processes possible using this system. By comparing the efficiency of constructs based on <it>Tribolium, Drosophila</it>, and artificial core promoters, respectively, we find that the use of endogenous core promoters is essential for high-level expression of transgenic constructs.</p> <p>Conclusions</p> <p>With the established GAL4/UAS binary expression system, ectopic misexpression approaches are now feasible in <it>Tribolium</it>. Our results support the contention that high-level transgene expression usually requires endogenous regulatory sequences, including endogenous core promoters in <it>Tribolium </it>and probably also other model systems.</p

Neuropsychological Functioning and Temperament Traits in a Czech Sample of Children and Adolescents at Familial Risk of Bipolar Disorder

Background: Although a positive family history is the strongest predictor for bipolar disorder (BD), most offspring of BD parents (BO) will not develop the disorder. Identification of vulnerability markers for BD is essential for specific individual risk estimation. Impairments in cognitive functioning and the presence of specific temperament traits are considered promising candidates.Methods: Sixty-three BO (48% female; 11.8 ± 3.3 years) and 54 control offspring (CO; 44% female; 12.3 ± 3.2 years) comparable in sex (p = 0.4) and age (p = 0.4) were enrolled. Detection of current sub/threshold mood symptoms by the Kiddie Schedule for Affective Disorders and Schizophrenia and General Behavior Inventory was applied to separate BO into ultrahigh-risk (UHR) and high-risk (HR) subgroups. Cognitive functions were tested by the Developmental Neuropsychological Assessment II test battery, d2 Test of Attention, and Amsterdam Neuropsychological Tasks. Temperament was assessed by the Temperament in Middle Childhood and Early Adolescent Temperament Questionnaires.Results: The BO sample consisted of 5 BD, 17 UHR, and 41 HR participants. We did not observe any significant differences between the BO and CO groups or between the UHR, HR, and CO subgroups (Hedges' g = 0.21–0.39) in cognitive functioning. The BO differed significantly in some temperament traits from the CO (g = 0.42–0.61), while the UHR subgroup exhibited lower effortful control and attention focusing than both HR and CO participants (g = 0.92–1.19).Limitations: The cross-sectional design and wide age range of the sample limited our findings.Conclusions: Neuropsychological impairment does not seem to be a trait marker of BD in the premorbid stage. Temperament with low effortful control and low attention focusing might be associated with the development of mood disorders in BO

Trace elements in glucometabolic disorders: an update

Many trace elements, among which metals, are indispensable for proper functioning of a myriad of biochemical reactions, more particularly as enzyme cofactors. This is particularly true for the vast set of processes involved in regulation of glucose homeostasis, being it in glucose metabolism itself or in hormonal control, especially insulin. The role and importance of trace elements such as chromium, zinc, selenium, lithium and vanadium are much less evident and subjected to chronic debate. This review updates our actual knowledge concerning these five trace elements. A careful survey of the literature shows that while theoretical postulates from some key roles of these elements had led to real hopes for therapy of insulin resistance and diabetes, the limited experience based on available data indicates that beneficial effects and use of most of them are subjected to caution, given the narrow window between safe and unsafe doses. Clear therapeutic benefit in these pathologies is presently doubtful but some data indicate that these metals may have a clinical interest in patients presenting deficiencies in individual metal levels. The same holds true for an association of some trace elements such as chromium or zinc with oral antidiabetics. However, this area is essentially unexplored in adequate clinical trials, which are worth being performed

The cadherin Fat2 is required for planar cell polarity in the Drosophila ovary

Planar cell polarity is an important characteristic of many epithelia. In the Drosophila wing, eye and abdomen, establishment of planar cell polarity requires the core planar cell polarity genes and two cadherins, Fat and Dachsous. Drosophila Fat2 is a cadherin related to Fat; however, its role during planar cell polarity has not been studied. Here, we have generated mutations in fat2 and show that Fat2 is required for the planar polarity of actin filament orientation at the basal side of ovarian follicle cells. Defects in actin filament orientation correlate with a failure of egg chambers to elongate during oogenesis. Using a functional fosmid-based fat2-GFP transgene, we show that the distribution of Fat2 protein in follicle cells is planar polarized and that Fat2 localizes where basal actin filaments terminate. Mosaic analysis demonstrates that Fat2 acts non-autonomously in follicle cells, indicating that Fat2 is required for the transmission of polarity information. Our results suggest a principal role for Fat-like cadherins during the establishment of planar cell polarity

Autistic traits modulate conscious and nonconscious face perception.

Difficulty with emotion perception is a core feature of autism spectrum disorder (ASD) that is also associated with the broader autism phenotype. The current study explored the neural underpinnings of conscious and nonconscious perceptions of affect in typically developing individuals with varying levels of autistic-like traits, as measured by the Autism Quotient (AQ). We investigated the relationship between autistic traits and face processing efficiency using event-related potentials (ERPs). In 20 typically developing adults, we utilized ERPs (the P100, N170, and P300) to measure differences in face processing for emotional faces that were presented either (a) too quickly to reach conscious awareness (16 ms) or (b) slowly enough to be consciously observed (200 ms). All individuals evidenced increased P100 and P300 amplitude and shorter N170 latencies for nonconscious versus consciously presented faces. Individuals with high AQ scores evidenced delayed ERP components. Nonconsciously perceived emotional faces elicited enhanced neural responses regardless of AQ score. Higher levels of autistic traits were associated with inefficient face perception (i.e., longer latency of ERP components). This delay parallels processing delays observed in ASD. These data suggest that inefficient social perception is present in individuals with subclinical levels of social impairment

Exome sequencing in a family with restless legs syndrome

Background: Restless legs syndrome (RLS) has a high familial aggregation. To date, several loci and genetic risk factors have been identified, but no causative gene mutation has been found