Identifying spatio-temporal dynamics of trace metals in shallow eutrophic lakes on the basis of a case study in Lake Taihu, China.

In shallow eutrophic lakes, metal remobilization is closely related to the resuspension and eutrophication. An improved understanding of metal dynamics by biogeochemical processes is essential for effective management strategies. We measured concentrations of nine metals (Cr, Cu, Zn, Ni, Pb, Fe, Al, Mg, and Mn) in water and sediments during seven periods from 2014 to 2018 in northern Lake Taihu, to investigate the metal pollution status, spatial distributions, mineral constituents, and their interactions with P. Moreover, an automatic weather station and online multi-sensor systems were used to measure meteorological and physicochemical parameters. Combining these measurements, we analyzed the controlling factors of metal dynamics. Shallow and eutrophic northern Lake Taihu presents more serious metal pollution in sediments than the average of lakes in Jiangsu Province. We found chronic and acute toxicity levels of dissolved Pb and Zn (respectively), compared with US-EPA "National Recommended Water Quality Criteria". Suspended particles and sediment have been polluted in different degrees from uncontaminated to extremely contaminated according to German pollution grade by LAWA (Bund/Länder-Arbeitsgemeinschaft Wasser). Polluted particles might pose a risk due to high resuspension rate and intense algal activity in shallow eutrophic lakes. Suspended particles have similar mineral constituents to sediments and increased with increasing wind velocity. Al, Fe, Mg, and Mn in the sediment were rarely affected by anthropogenic pollution according to the geoaccumulation index. Among them, Mn dynamics is very likely associated with algae. Micronutrient uptake by algal will affect the migration of metals and intensifies their remobilization. Intensive pollution of most particulate metals were in the industrialized and down-wind area, where algae form mats and decompose. Moreover, algal decomposition induced low-oxygen might stimulate the release of metals from sediment. Improving the eutrophication status, dredging sediment, and salvaging cyanobacteria biomass are possible ways to remove or reduce metal contaminations.

Nosip functions during vertebrate eye and cranial cartilage development.

BACKGROUND: The nitric oxide synthase interacting protein (Nosip) has been associated with diverse human diseases including psychological disorders. In line, early neurogenesis of mouse and Xenopus is impaired upon Nosip deficiency. Nosip knockout mice show craniofacial defects and the down-regulation of Nosip in the mouse and Xenopus leads to microcephaly. Until now, the exact underlying molecular mechanisms of these malformations were still unknown. RESULTS: Here, we show that nosip is expressed in the developing ocular system as well as the anterior neural crest cells of Xenopus laevis. Furthermore, Nosip inhibition causes severe defects in eye formation in the mouse and Xenopus. Retinal lamination as well as dorso-ventral patterning of the retina were affected in Nosip-depleted Xenopus embryos. Marker gene analysis using rax, pax6 and otx2 reveals an interference with the eye field induction and differentiation. A closer look on Nosip-deficient Xenopus embryos furthermore reveals disrupted cranial cartilage structures and an inhibition of anterior neural crest cell induction and migration shown by twist, snai2, and egr2. Moreover, foxc1 as downstream factor of retinoic acid signalling is affected upon Nosip deficiency. CONCLUSIONS: Nosip is a crucial factor for the development of anterior neural tissue such the eyes and neural crest cells. Developmental Dynamics 247:1070-1082, 2018. © 2018 Wiley Periodicals, Inc.

Developmental neurogenesis in mouse and Xenopus is impaired in the absence of Nosip.

BACKGROUND: Genetic deletion of Nosip in mice causes holoprosencephaly, however, the function of Nosip in neurogenesis is currently unknown. RESULTS: We combined two vertebrate model organisms, the mouse and the South African clawed frog, Xenopus laevis, to study the function of Nosip in neurogenesis. We found, that size and cortical thickness of the developing brain of Nosip knockout mice were reduced. Accordingly, the formation of postmitotic neurons was greatly diminished, concomitant with a reduced number of apical and basal neural progenitor cells in vivo. Neurospheres derived from Nosip knockout embryos exhibited reduced growth and the differentiation capability into neurons in vitro was almost completely abolished. Mass spectrometry analysis of the neurospheres proteome revealed a reduced expression of Rbp1, a regulator of retinoic acid synthesis, when Nosip was absent. We identified the homologous nosip gene to be expressed in differentiated neurons in the developing brain of Xenopus embryos. Knockdown of Nosip in Xenopus resulted in a reduction of brain size that could be rescued by reintroducing human NOSIP mRNA. Furthermore, the expression of pro-neurogenic transcription factors was reduced and the differentiation of neuronal cells was impaired upon Nosip knockdown. In Xenopus as well as in mouse we identified reduced proliferation and increased apoptosis as underlying cause of microcephaly upon Nosip depletion. In Xenopus Nosip and Rbp1 are similarly expressed and knockdown of Nosip resulted in down regulation of Rbp1. Knockdown of Rbp1 caused a similar microcephaly phenotype as the depletion of Nosip and synergy experiments indicated that both proteins act in the same signalling pathway. CONCLUSIONS: Nosip is a novel factor critical for neural stem cell/progenitor self-renewal and neurogenesis during mouse and Xenopus development and functions upstream of Rbp1 during early neurogenesis.