Background: Multiple studies have shown that brain gene expression is disturbed in subjects suffering from schizophrenia. However, disentangling disease effects from alterations caused by medication is a challenging task. The main goal of this study is to find transcriptional alterations in schizophrenia that are independent of neuroleptic treatment.

The quaking viable mouse mutation (qk v ) is a deletion including the 5 regulatory region of the quaking gene (Qki), which causes body tremor and severe dysmyelination in mouse. The function of the human quaking gene, called quaking homolog KH domain RNAbinding (mouse) (QKI), is not well known. We have previously shown that QKI is a new candidate gene for schizophrenia. Here we show that human QKI mRNA levels can account for a high proportion (47%) of normal interindividual mRNA expression variation (and covariation) of six oligodendrocyte-related genes (PLP1, MAG, MBP, TF, SOX10, and CDKN1B) in 55 human brain autopsy samples from individuals without psychiatric diagnoses. In addition, the tightly coexpressed myelin-related genes (PLP1, MAG, and TF) have decreased mRNA levels in 55 schizophrenic patients, as compared with 55 control individuals, and most of this difference (68 -96%) can be explained by variation in the relative mRNA levels of QKI-7kb, the same QKI splice variant previously shown to be down-regulated in patients with schizophrenia. Taken together, our results suggest that QKI levels may regulate oligodendrocyte differentiation and maturation in human brain, in a similar way as in mouse. Moreover, we hypothesize that previously observed decreased activity of myelin-related genes in schizophrenia might be caused by disturbed QKI splicing.myelin ͉ quaking ͉ splice variant

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Sporadic summer rainfall in semi-arid ecosystems can provide enough soil moisture to drastically increase CO(2) efflux and rates of soil N cycling. The magnitudes of C and N pulses are highly variable, however, and the factors regulating these pulses are poorly understood. We examined changes in soil respiration, bacterial, fungal and microfaunal populations, and gross rates of N mineralization, nitrification, and NH(4) (+) and NO(3) (-) immobilization during the 10 days following wetting of dry soils collected from stands of big sagebrush (Artemisia tridentata) and cheatgrass (Bromus tectorum) in central Utah. Soil CO(2) production increased more than tenfold during the 17 h immediately following wetting. The labile organic C pool released by wetting was almost completely respired within 2-3 days, and was nearly three times as large in sagebrush soil as in cheatgrass. In spite of larger labile C pools beneath sagebrush, microbial and microfaunal populations were nearly equal in the two soils. Bacterial and fungal growth coincided with depletion of labile C, and populations peaked in both soils 2 days after wetting. Protozoan populations, whose biomass was nearly 3,000-fold lower than bacteria and fungi, peaked after 2-4 days. Gross N mineralization and nitrification rates were both faster in cheatgrass soil than in sagebrush, and caused greater nitrate accumulation in cheatgrass soil. Grazing of bacteria and fungi by protozoans and nematodes could explain neither temporal trends in N mineralization rates nor differences between soil types. However, a mass balance model indicated that the initial N pulse was associated with degradation of microbial substrates that were rich in N (C:N <8.3), and that microbes had shifted to substrates with lower N contents (C:N =15-25) by day 7 of the incubation. The model also suggested that the labile organic matter in cheatgrass soil had a lower C:N ratio than in sagebrush, and this promoted faster N cycling rates and greater N availability. This study provides evidence that the high N availability often associated with wetting of cheatgrass soils is a result of cheatgrass supplying substrates to microbes that are of high decomposability and N content.