CgIPT1 is required for synthesis of cis-zeatin cytokinins and contributes to stress tolerance and virulence in Colletotrichum graminicola.

We have previously shown that the maize pathogen Colletotrichum graminicola is able to synthesise cytokinins (CKs). However, it remained unsettled whether fungal CK production is essential for virulence in this hemibiotrophic fungus. Here, we identified a candidate gene, CgIPT1, that is homologous to MOD5 of Saccharomyces cerevisiae and genes from other fungi and plants, which encode tRNA-isopentenyltransferases (IPTs). We show that the wild type strain mainly synthesises cis-zeatin-type (cisZ) CKs whereas ΔCgipt1 mutants are severely impeded to do so. The spectrum of CKs produced confirms bioinformatical analyses predicting that CgIpt1 is a tRNA-IPT. The virulence of the ΔCgipt1 mutants is moderately reduced. Furthermore, the mutants exhibit increased sensitivities to osmotic stress imposed by sugar alcohols and salts, as well as cell wall stress imposed by Congo red. Amendment of media with CKs did not reverse this phenotype suggesting that fungal-derived CKs do not explain the role of CgIpt1 in mediating abiotic stress tolerance. Moreover, the mutants still cause green islands on senescing maize leaves indicating that the cisZ-type CKs produced by the fungus do not cause this phenotype.

Selecting and defining indicators for diabetes surveillance in Germany.

Mainly because of the large number of people affected and associated significant health policy implications, the Robert Koch Institute (RKI) is developing a public health surveillance system using diabetes as an example. In a first step to ensure long-term and comparable data collection and establish efficient surveillance structures, the RKI has defined a set of relevant indicators for diabetes surveillance. An extensive review of the available literature followed by a structured process of consensus provided the basis for a harmonised set of 30 core and 10 supplementary indicators. They correspond to the following four fields of activity: (1) reducing diabetes risk, (2) improving diabetes early detection and treatment, (3) reducing diabetes complications, (4) reducing the disease burden and overall costs of the disease. In future, in addition to the primary data provided by RKI health monitoring diabetes surveillance needs to also consider the results from secondary data sources. Currently, barriers to accessing this data remain, which will have to be overcome, and gaps in the data closed. The RKI intentends to continuously update this set of indicators and at some point apply it also to further chronic diseases with high public health relevance.

Gestational Diabetes Impairs Human Fetal Postprandial Brain Activity.

CONTEXT: Gestational diabetes (GDM) influences the fetal phenotype. OBJECTIVE: In the present study, our aim was to determine the effect of GDM specifically on fetal brain activity. DESIGN: Pregnant participants underwent an oral glucose tolerance test (OGTT, 75 g). At 0, 60, and 120 minutes, maternal metabolism was determined, and fetal auditory evoked fields were recorded with a fetal magnetoencephalographic device. SETTING: All measurements were performed at the fMEG Center in Tübingen. PARTICIPANTS: Twelve women with GDM and 28 normal glucose-tolerant (NGT) pregnant women participated on a voluntary basis. INTERVENTIONS: OGTT (75 g, 120 minutes) was used in this study. MAIN OUTCOMES AND MEASURES: Fetal auditory evoked response latencies were determined for this study. RESULTS: In the fetuses of NGT women, latencies decreased between 0 and 60 minutes from 260 ± 90 to 206 ± 74 ms (P = .008) and remained stable until 120 minutes (206 ± 74 vs 230 ± 79, P =.129). In fetuses of women with GDM, there was no change in response latencies during OGTT (P = .11). Sixty minutes after glucose ingestion, fetal latencies in the GDM group were longer than in the NGT group (296 ± 82 vs 206 ± 74 ms, P = .001). Linear regression revealed a significant effect of maternal glucose, insulin levels, and insulin sensitivity on response latencies after 60 minutes. CONCLUSIONS: Fetal postprandial brain responses were slower in the offspring of women with GDM. This might indicate that gestational diabetes directly affects fetal brain development and may lead to central nervous insulin resistance in the fetus.