Transgenic Xenopus embryos reveal that anterior neural development requires continued suppression of BMP signaling after gastrulation.

In vertebrates, BMP signaling before gastrulation suppresses neural development. Later in development, BMP signaling specifies a dorsal and ventral fate in the forebrain and dorsal fate in the spinal cord. It is therefore possible that a change in the competence of the ectoderm to respond to BMP signaling occurs at some point in development. We report that exposure of the anterior neural plate to BMP4 before gastrulation causes suppression of all neural markers tested. To determine the effects of BMP4 after gastrulation, we misexpressed BMP4 using a Pax-6 promoter fragment in transgenic frog embryos and implanted beads soaked in BMP4 in the anterior neural plate. Suppression of most anterior neural markers was observed. We conclude that most neural genes continue to require suppression of BMP signaling into the neurula stages. Additionally, we report that BMP4 and BMP7 are abundantly expressed in the prechordal mesoderm of the neurula stage embryo. This poses the paradox of how the expression of most neural genes is maintained if they can be inhibited by BMP signaling. We show that at least one gene in the anterior neural plate suppresses the response of the ectoderm to BMP signaling. We propose that the suppressive effect of BMP signaling on the expression of neural genes coupled with localized suppressors of BMP signaling result in the fine-tuning of gene expression in the anterior neural plate.     

Synthesis of certain 2'-deoxyuridine derivatives containing substituted phenoxy groups attached to C-5'; evaluation as potential dUTP analogues

Derivatives of 2'-deoxyuridine in which the 5'-OH group is replaced by a 2,3,6-trifluoro-5-hydroxy-4-nitrophenoxy or a 4-carboxy-2,3,6-trifluoro-5-hydroxyphenoxy group have been prepared for evaluation as possible dUTP analogues. They showed a weak ability to displace radiolabelled dUTP from a dUTP-binding antiserum. The corresponding compounds lacking the three fluorine substituents were prepared for comparison.     

Diaphyseal medullary stenosis with malignant fibrous histiocytoma: a hereditary bone dysplasia/cancer syndrome maps to 9p21-22

Diaphyseal medullary stenosis with malignant fibrous histiocytoma (DMS-MFH) is an autosomal dominant bone dysplasia/cancer syndrome of unknown etiology. This rare hereditary cancer syndrome is characterized by bone infarctions, cortical growth abnormalities, pathological fractures, and eventual painful debilitation. Notably, 35% of individuals with DMS develop MFH, a highly malignant bone sarcoma. A genome scan for the DMS-MFH gene locus in three unrelated families with DMS-MFH linked the syndrome to a region of approximately 3 cM on chromosome 9p21-22, with a maximal two-point LOD score of 5.49 (marker D9S171 at recombination fraction [theta].05). Interestingly, this region had previously been shown to be the site of chromosomal abnormalities in several other malignancies and contains a number of genes whose protein products are involved in growth regulation. Identification of this rare familial sarcoma-causing gene would be expected to simultaneously define the cause of the more common nonfamilial, or sporadic, form of MFH-a tumor that constitutes approximately 6% of all bone cancers and is the most frequently occurring adult soft-tissue sarcoma.     

Photosynthetic activities of cadmium-treated tomato plants

Tomato plants (Lycopersicum esculentum Mill. cv. Moneymaker) grown on nutrient medium containing cadmium exhibit reduced net photosynthesis and reduced contents of chlorophyll and accessory pigments. In chloroplasts isolated from cadmiumtreated plants photosystem II activity, as measured by 2,6-dichlorophenolindophenol photoreduction, and photosystem II + I activity (H₂O → methyl viologen) were both inhibited to about 60%. When 1,5-diphenylcarbazide was used as artificial electron donor, no significant cadmium effect was observed. Photosystem I activity was not affected by cadmium. The fine structure of chloroplasts in cadmium-treated plants was degenerated, similarly to senescence response. The principal symptom of cadmium action was the occurrence of large plastoglobules and a disorganization of the lamellar structure, mainly grana stacks. Transfer of cadmium-treated plants into a medium with increased manganese level caused grana stacking and restoration of photosystem II activity.     

No regulatory role for adult predation in cyclic population dynamics of the autumnal moth,Epirrita autumnata

1. Multiannual population cycles of geometrid moths are thought to be driven by trophic‐level interactions involving a delayed density‐dependent component. Predation on adult moths has been a little‐studied mechanism of this phenomenon. 2. Using 29 daytime and 61 night‐time predation trials in the field, we exposed living autumnal moth (Epirrita autumnata Borkhausen, Lepidoptera: Geometridae) females to their natural predators during each autumn throughout the 10‐year population cycle. 3. In our northern study location (70°N), insectivorous passerines had already migrated, and harvestman Mitopus morio Fabricius (Opiliones: Phalangiidae) was found to be the main predator of the adult moths. The predation mortality occurred mainly at night and was positively correlated with the minimum temperature measured during the predation trial. 4. Despite high annual variability in the degree of adult predation, both direct and delayed density‐dependent effects were weak and indicate that predation on adult moths in the autumn does not have any regulatory role in cyclic population dynamics of the autumnal moth in northern Fennoscandia.     

Hot spots for nitrous oxide emissions found in different types of permafrost peatlands

Recent findings on large nitrous oxide (N₂O) emissions from permafrost peatlands have shown that tundra soils can support high N₂O release, which is on the contrary to what was thought previously. However, field data on this topic have been very limited, and the spatial and temporal extent of the phenomenon has not been known. To address this question, we studied N₂O dynamics in two types of subarctic permafrost peatlands, a peat plateau in Russia and three palsa mires in Finland, including also adjacent upland soils. The peatlands studied have surfaces that are uplifted by frost (palsas and peat plateaus) and partly unvegetated as a result of wind erosion and frost action. Unvegetated peat surfaces with high N₂O emissions were found from all the studied peatlands. Very high N₂O emissions were measured from peat circles at the Russian site (1.40±0.15 g N₂O m^?2 yr^?1). Elevated, sparsely vegetated peat mounds at the same site had significantly lower N₂O release. The N₂O emissions from bare palsa surfaces in Northern Finland were highly variable but reached high rates, similar to those measured from the peat circles. All the vegetated soils studied had negligible N₂O release. At the bare peat surfaces, the large N₂O emissions were supported by the absence of plant N uptake, the low C : N ratio of the peat, the relatively high gross N mineralization rate and favourable moisture content, together increasing availability of mineral N for N₂O production. We hypothesize that frost heave is crucial for high N₂O emissions, since it lifts the peat above the water table, increasing oxygen availability and making it vulnerable to the the physical processes that may remove the vegetation cover. In the future, permafrost thawing may change the distribution of wet and dry surfaces in permafrost peatlands, which will affect N₂O emissions.     

FGF-8 stimulates neuronal differentiation through FGFR-4a and interferes with mesoderm induction in Xenopus embryos

The role of fibroblast growth factors (FGFs) in neural induction is controversial [1,2]. Although FGF signalling has been implicated in early neural induction [3-5], a late role for FGFs in neural development is not well established. Indeed, it is thought that FGFs induce a precursor cell fate but are not able to induce neuronal differentiation or late neural markers [6-8]. It is also not known whether the same or distinct FGFs and FGF receptors (FGFRs) mediate the effects on mesoderm and neural development. We report that Xenopus embryos expressing ectopic FGF-8 develop an abundance of ectopic neurons that extend to the ventral, non-neural, ectoderm, but show no ectopic or enhanced notochord or somitic markers. FGF-8 inhibited the expression of an early mesoderm marker, Xbra, in contrast to eFGF, which induced ectopic Xbra robustly and neuronal differentiation weakly. The effect of FGF-8 on neurogenesis was blocked by dominant-negative FGFR-4a (DeltaXFGFR-4a). Endogenous neurogenesis was also blocked by DeltaXFGFR-4a and less efficiently by dominant-negative FGFR-1 (XFD), suggesting that it depends preferentially on signalling through FGFR-4a. The results suggest that FGF-8 and FGFR-4a signalling promotes neurogenesis and, unlike other FGFs, FGF-8 interferes with mesoderm induction. Thus, different FGFs show specificity for mesoderm induction versus neurogenesis and this may be mediated, at least in part, by the use of distinct receptors.     

Unfolding retinal dystrophies: a role for molecular chaperones?

Inherited retinal dystrophy is a major cause of blindness worldwide. Recent molecular studies have suggested that protein folding and molecular chaperones might play a major role in the pathogenesis of these degenerations. Incorrect protein folding could be a common consequence of causative mutations in retinal degeneration disease genes, particularly mutations in the visual pigment rhodopsin. Furthermore, several retinal degeneration disease genes have recently been identified as putative facilitators of correct protein folding, molecular chaperones, on the basis of sequence homology. We also consider whether manipulation of chaperone levels or chaperone function might offer potential novel therapies for retinal degeneration.