Chlorinity determination in estuarine waters by physical measurement

The differential refractometer has been used as an effective instrument for chlorinity determination. Results obtained through its application have been compared with those derived from the use of less sensitive refractometers and with those obtained from specific conductivity measurements. The advantages of differential refractive-index measurements when applied to water in an estuarial brackish marsh basin are demonstrated...

The transcription factors, Scl and Lmo2, act together during development of the haemangioblast in zebrafish

The transcription factors, Scl and Lmo2, are crucial for development of all blood. An important early requirement for Scl in endothelial development has also been revealed recently in zebrafish embryos, supporting previous findings in scl(-/-) embryoid bodies. Scl depletion culminates most notably in failure of dorsal aorta formation, potentially revealing a role in the formation of haemogenic endothelium. We now present evidence that the requirements for Lmo2 in zebrafish embryos are essentially the same as for Scl. The expression of important haematopoietic regulators is lost, reduced or delayed, pan-endothelial gene expression is downregulated and aorta-specific marker expression is lost. The close similarity of the phenotypes for Scl and Lmo2 suggest that they perform these early functions in haemangioblast development within a multi-protein complex, as shown for erythropoiesis. Consistent with this, we find that Scl morphants cannot be rescued by a non-Lmo2 binding form of Scl but can be rescued by non-DNA binding forms, suggesting tethering to target genes through DNA-binding partners linked via Lmo2. Interestingly, unlike other haematopoietic regulators, the Scl/Lmo2 complex does not appear to autoregulate as neither gene's expression is affected by depletion of the other. Thus, expression of these critical regulators is dependent on continued expression of upstream regulators, which may include cell extrinsic signals.status: publishe

Genetic therapy in a mitochondrial disease model suggests a critical role for liver dysfunction in mortality

The clinical and largely unpredictable heterogeneity of phenotypes in patients with mitochondrial disorders demonstrates the ongoing challenges in the understanding of this semi-autonomous organelle in biology and disease. Previously, we used the gene-breaking transposon to create 1200 transgenic zebrafish strains tagging protein-coding genes (Ichino et al., 2020), including the lrpprc locus. Here, we present and characterize a new genetic revertible animal model that recapitulates components of Leigh Syndrome French Canadian Type (LSFC), a mitochondrial disorder that includes diagnostic liver dysfunction. LSFC is caused by allelic variations in the LRPPRC gene, involved in mitochondrial mRNA polyadenylation and translation. lrpprc zebrafish homozygous mutants displayed biochemical and mitochondrial phenotypes similar to clinical manifestations observed in patients, including dysfunction in lipid homeostasis. We were able to rescue these phenotypes in the disease model using a liver-specific genetic model therapy, functionally demonstrating a previously under-recognized critical role for the liver in the pathophysiology of this disease