Forest Clearance and Fragmentation in Palawan and Eastern Mindanao Biodiversity Corridors (1990-2000): A Time Sequential Analysis of LANDSAT Imagery

Conservation International has mapped changes in forest cover in the Philippines over large areas in two biodiversity corridors, as defined by the Critical Ecosystems Partnership Fund (CEPF). These changes were derived by analysing Landsat satellite imagery at a spatial resolution of 28.5 m. The dataset analysed includes Landsat 5 data from circa 1990 (+/- 3 years) and Landsat 7 data from circa 2000. Image dates were determined based on the availability of free, nearly cloud-free imagery from the University of Maryland’s Global Land Cover Facility (http://glcf.umiacs.umd.edu/index.shtml). Additional scenes were also purchased for areas most heavily covered with clouds. A supervised classification approach was employed, using a decision tree classifier. The total amount of forest cleared during the time period was 20.1 km2 in the Eastern Mindanao corridor and 37.5 km2 in the Palawan biodiversity corridor, representing an average annual forest clearance rate of 0.04 percent for Eastern Mindanao and 0.07 percent for Palawan.   Forest fragmentation was also observed to be more apparent in Palawan due to clearance of smaller forest patches.  Forest cover interpretation from the Landsat imagery was validated through a collective aerial system of videography and photography. The combined accuracy of the classified maps was 85.4 percent

Loss of CBY1 results in a ciliopathy characterized by features of Joubert syndrome

Ciliopathies are clinically and genetically heterogeneous diseases. We studied three patients from two independent families presenting with features of Joubert syndrome: abnormal breathing pattern during infancy, developmental delay/intellectual disability, cerebellar ataxia, molar tooth sign on magnetic resonance imaging scans, and polydactyly. We identified biallelic loss-of-function (LOF) variants in CBY1, segregating with the clinical features of Joubert syndrome in the families. CBY1 localizes to the distal end of the mother centriole, contributing to the formation and function of cilia. In accordance with the clinical and mutational findings in the affected individuals, we demonstrated that depletion of Cby1 in zebrafish causes ciliopathy-related phenotypes. Levels of CBY1 transcript were found reduced in the patients compared with controls, suggesting degradation of the mutated transcript through nonsense-mediated messenger RNA decay. Accordingly, we could detect CBY1 protein in fibroblasts from controls, but not from patients by immunofluorescence. Furthermore, we observed reduced ability to ciliate, increased ciliary length, and reduced levels of the ciliary proteins AHI1 and ARL13B in patient fibroblasts. Our data show that CBY1 LOF-variants cause a ciliopathy with features of Joubert syndrome

Nitratherkunft im Bodenwasser und Grundwasser = Origine des nitrates dans l'eau du sol et les eaux souterraines

Untersuchungsgebiet unteres Birstal zwischen Reinach und Aesc

Nachweis und Interpretation von Grundwasserschwankungen in einem flussnahen Trinkwasserfördergebiet mittels multivariater Analyse

Hydrogeologie der Nordwestschweiz, Grundwasse

A Complex of BBS1 and NPHP7 Is Required for Cilia Motility in Zebrafish

<div><p>Bardet-Biedl syndrome (BBS) and nephronophthisis (NPH) are hereditary autosomal recessive disorders, encoded by two families of diverse genes. BBS and NPH display several overlapping phenotypes including cystic kidney disease, retinitis pigmentosa, liver fibrosis, <i>situs inversus</i> and cerebellar defects. Since most of the BBS and NPH proteins localize to cilia and/or their appendages, BBS and NPH are considered ciliopathies. In this study, we characterized the function of the transcription factor Nphp7 in zebrafish, and addressed the molecular connection between BBS and NPH. The knockdown of zebrafish <i>bbs1</i> and <i>nphp7.2</i> caused similar phenotypic changes including convergent extension defects, curvature of the body axis, hydrocephalus, abnormal heart looping and cystic pronephros, all consistent with an altered ciliary function. Immunoprecipitation assays revealed a physical interaction between BBS1 and NPHP7, and the simultaneous knockdown of z<i>bbs1</i> and z<i>nphp7.2</i> enhanced the cystic pronephros phenotype synergistically, suggesting a genetic interaction between z<i>bbs1</i> and z<i>nphp7.2 in vivo</i>. Deletion of zBbs1 or zNphp7.2 did not compromise cilia formation, but disrupted cilia motility. Although NPHP7 has been shown to act as transcriptional repressor, our studies suggest a crosstalk between BBS1 and NPHP7 in regulating normal function of the cilium.</p></div

Knockdown of <i>znphp7.2</i> showed normal development of cilia.

<p>(A) Images of live zebrafish embryos at the 8–10 somite stage. Kupffer's vesicle is located in the dashed box. (B) Measurement of relative KV area with setting control as ‘1.00’. The knockdown of z<i>nphp7.2</i> did not significantly affect on KV development and area. (C) Images of cilia in the KV of 8–10 somite stage were stained for acetylated tubulin. Scale bar = 10 µm. (D) zNphp7.2-deficient embryos showed shortened length of cilia in KV compared to control embryos. (E) Staining of acetylated tubulin in the anterior pronephric tubule of morphants at 48 hpf displayed that the overall distribution of cilia remained unchanged compared to control (Scale bar = 10 µm) even though (F) the knockdown either of z<i>bbs1</i> showed longer and the knockdown of z<i>nphp7.2</i> showed shorter cilia. (PT, Pronephric Tubule) (G and H) The morphology and length of cilia in posterior pronephric tubule appeared unchanged in combined knockdown of z<i>bbs1</i> and z<i>nphp7.2</i> compared to single knockdown of z<i>bbs1</i> or z<i>nphp7.2</i> or compared to Cont MO injected embryos. (PT, Pronephric Tubule) (I) The morphants of z<i>bbs1</i> and z<i>nphp7.2</i> displayed normal ultrastructure of motile cilia in pronephric tubule without recognizable deficiency in dynein arms (outer dynein arm marked by arrowhead). The numbers (n) in the graphs are the number of total cilia which were examined. 4–6 individual embryos per group were examined.</p

Expression of z<i>bbs1</i> and z<i>nphp7</i>.

<p>(A) Identification of 2 NPHP7 homologues in zebrafish: Zebrafish Nphp7.1 (zNphp7.1) and zebrafish Nphp7.2 (zNphp7.2) consist of 446 and 489 amino acids respectively. Amino acid sequence alignment showed that zNphp7.1 shares 43.9% identity and 50.8% similarity with the human NPHP7/GLIS2 (hNPHP7); zNphp7.2 was 51.4% identical and 60.2% similar to the human homologue. The ZF domains of zNphp7.1 and zNphp7.2 were 89.3% and 91.3% identical with those of the human homologue, respectively. (<b>*</b>, completely conserved; <b>.</b>, identical in 2 sequences or belonging to same type of amino acid group in 2 or 3 sequences) (B) Semi-quantitative RT-PCR reveals maternal transcript expression for z<i>nphp7.1</i> and z<i>nphp7.2</i> whereas z<i>bbs1</i> is not expressed maternally nor at 6 hpf. 2 maternal splice products were identified for z<i>nphp7.2</i> (open arrowhead: Transcript 1; filled arrowhead: Transcript 2). The transcript 2 of z<i>nphp7.2</i> is expressed only maternally. Sequencing of the lower splice product revealed an excision of 18 bp corresponding to amino acid (aa 101–118) (<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0072549#pone.0072549.s001" target="_blank">Fig. S1</a>). (C) Semi-quantitative RT-PCR with organ specific cDNA from adult zebrafish indicated that z<i>bbs1</i> is expressed in kidney, eye and testis. z<i>nphp7.1</i> and z<i>nphp7.2</i> are expressed in other organs including kidney, eye, heart, testis, gut and muscle.</p

Genetic interaction between z<i>bbs1</i> and z<i>nphp7.2 in vivo</i>.

<p>Injected zebrafish embryos were assessed for the incidence of pronephric cysts. (A) Cont MO injected embryos with normal pronephros. While the majority of z<i>bbs1</i> or z<i>nphp7.2</i> morphants (suboptimal dose) showed pronephros of normal morphology, those of combined knockdown exhibited pronephros with cysts. Cysts are marked by asterisks. (Black scale bar = 500 µm, White scale bar = 100 µm) (B) Pronephric cysts were detectable after individual injections of <i>znphp7.2</i> MO at 0.1 mM and <i>zbbs1</i> MO at 0.2 mM with the level of 17% and 10% respectively whereas the combined knockdown caused pronephric cysts in 59% of microinjected embryos. The final MO concentration for injection was 0.3 mM in all conditions to keep total MO dose constant. Therefore suboptimal doses of z<i>bbs1</i> and z<i>nphp7.2</i> MO were combined with Cont MO to obtain this final concentration of 0.3 mM. The numbers in the brackets (n) are the numbers of total embryos which were examined.</p