The ecological impact and management of an invasive species – the American mink

Den Amerikanska minken (Neovison vison) är troligen främst känd för att vara ett djur som föds upp inom pälsindustrin för dess eftertraktade skinn, men minken har även en roll i ekosystemet. När minken befinner sig utanför sitt hemland utgör den däremot ett hot mot ett flertal arter, vilket är viktigt att ta hänsyn till för att bevara den biologiska mångfalden. Minken lever naturligt i skogarna i Nordamerika, där den jagas för sin päls. I början av 1900-talet började minken födas upp i fångenskap för pälsens skull. Senare under 1900-talet importerades minken både till Storbritannien, Europa och Norden för att födas upp inom pälsindustrin. Genom att minkar sedan släppts ut eller rymt från pälsfarmarna, och dessutom är väldigt anpassningsbara har de nu etablerat sig i hela Norden och större delar av Europa, samt Storbritannien. Minken har påverkat antalet grodor, vattensorkar och sjöfåglar negativt i dessa länder, särskilt i skärgården men även på fastlandet. En mink kan räcka för att förstöra fåglarnas häckning på en ö både genom att döda sjöfåglar och genom att äta deras ägg. Dessutom har minkens setts konkurrera med och döda flodillern, trots att de nästan är lika stora. Den biologiska mångfalden sjunker redan idag och ett flertal arter håller på att dö ut. Närvaron av invasiva arter som mink tillsammans med klimatförändringar, och förlorade naturmiljöer bidrar ytterligare till en förlorad biologisk mångfald. Lyckligtvis finns det fortfarande hopp. Ett flertal projekt har utförts för att minska minkens påverkan på hotade arter. Till exempel kan bevarande av naturmiljöer som små vattendrag och vassbäddar skydda vattensorken från minken, samtidigt som en tät växtlighet på öar kan skydda grodorna. En framtida möjlighet kan även vara att bygga konstgjorda vassbäddar för att bevara den biologiska mångfalden. I vissa länder har dessutom utterns återkomst kunnat hämma minkens spridning genom att konkurrera med den.The American mink (Neovison vison) is an invasive species native to North America, that has now become widespread in Europe and the British Isles through escape and release from fur farms. The species is difficult to control because of its phenotypic plasticity and its adaptability to new environments. The purpose of this literature review was therefore to investigate what ecological impact the mink has on other species, and possible solutions to minimize it. Moreover, advantages and disadvantages with different detecting and trapping methods were evaluated in order to asses which method that is most beneficial. Different management strategies are also discussed. The results of this study suggest that the American mink has a negative ecological impact on other species like birds, frogs and water voles by reducing their population density, both on archipelagos and at the mainland. Moreover, the American mink may serve as a threat to the European mink (Mustela lutreola) by competition. The American mink´s negative impact on biodiversity may be mitigated through preserving certain habitats that protect prey species, reintroduction of the native otter (Lutra lutra) and by managing invasive prey species that are important food sources to the mink. The most beneficial method to detect and trap mink was the use of mink rafts in combination with live traps. This way control efforts and working force will be reduced, especially during long control projects, and killing of non-target animals will be minimized. GoodNature Self resetting traps may be resource effective in the future, but more scientific validation is warranted on how to minimize killing of non-target animals with this trap. To conclude, the most effective control strategies in order to protect threatened species would be to focus the control efforts on areas where the mink is within proximity to these species, and to kill female mink and juveniles during autumn. The most resource effective and successful strategy to control the feral mink is an adaptive management approach, especially when information about the target population is scarce

Assessment of extraction variables on agar gelling properties from cultural alga (Gracilariopsis persica) by RSM

In this present, response surface methodology was used to investigate the procedure of agar gelling properties from Gracilariopsis persica agarophyte and optimization them formulation. Base on result, three independent variables - alkalinity concentration (2-8%), extraction temperature (90-120°C) and extraction time (45-240 minutes) - in five levels on viscosity and hysteresis temperature were determined that effects of extraction time and temperature on viscosity and hysteresis temperature were significant (p0.05)

An intronic alteration of the fibroblast growth factor 10 gene causing ALSG-(aplasia of lacrimal and salivary glands) syndrome

<p>Abstract</p> <p>Background</p> <p>A combined aplasia, hypoplasia or atresia of lacrimal points and salivary glands is rarely diagnosed. Those patients suffer from epiphora, xerostomia and severe dental caries. This phenotype represents the autosomal-dominant aplasia of lacrimal and salivary glands syndrome (ALSG). Recently, aberrations of the <it>Fibroblast Growth Factor 10 </it>(<it>FGF10</it>) gene have been identified to be causative for this disorder.</p> <p>Methods</p> <p>We performed a sequence analysis of the <it>FGF10 </it>gene of a patient with ALSG-syndrome and his also affected brother as well as 193 controls. The FGF10 transcript was analyzed using RNA extracted from primary fibroblasts of the patient's mucosa.</p> <p>Results</p> <p>We detected a novel heterozygous sequence variation in intron 2 (c.430-1, G > A) causing the ALSG syndrome. The alteration derogates the regular splice acceptor site and leads to the use of a new splice acceptor site 127 bp upstream of exon 3. The aberration was detected in the genomic DNA derived from two affected brothers, but not in 193 control individuals. Furthermore, no diseased member of the family displayed additional abnormalities that are indicative for the clinically overlapping lacrimo-auriculo-dento-digital syndrome (LADD).</p> <p>Conclusion</p> <p>This family-based approach revealed an intronic variation of the <it>FGF10 </it>gene causing ALSG-syndrome. Our results expand the mutational and clinical spectrum of the ALSG syndrome.</p

Interrogation of a lacrimo-auriculo-dento-digital syndrome protein reveals novel modes of fibroblast growth factor 10 (FGF10) function

Heterozygous mutations in the gene encoding fibroblast growth factor 10 (FGF10) or its cognate receptor, FGF-receptor 2 IIIb (FGFR2-IIIb) result in two human syndromes - LADD (lacrimo-auriculo-dento-digital) and ALSG (Aplasia of lacrimal and salivary glands). To date, the partial loss-of-FGF10 function in these patients has been attributed solely to perturbed paracrine signalling functions between FGF10-producing mesenchymal cells and FGF10-responsive epithelial cells. However, the functioning of a LADD-causing G138E FGF10 mutation, which falls outside its receptor interaction interface, has remained enigmatic. In this study, we interrogated this mutation in the context of FGF10's protein sequence and three-dimensional structure, and followed the subcellular fate of tagged proteins containing this or other combinatorial FGF10 mutations, in vitro. We report that FGF10 harbours two putative nuclear localization sequences, termed NLS1 and NLS2, which individually or co-operatively promote nuclear translocation of FGF10. Furthermore, FGF10 localizes to a subset of dense fibrillar components of the nucleolus. G138E falls within NLS1 and abrogates FGF10's nuclear translocation whilst attenuating its progression along the secretory pathway. Our findings suggest that in addition to its paracrine roles, FGF10 may normally play intracrine role/s within FGF10-producing cells. Thus, G138E may disrupt both paracrine and intracrine function/s of FGF10 through attenuated secretion and nuclear translocation, respectively

ISL1 Directly Regulates FGF10 Transcription during Human Cardiac Outflow Formation

The LIM homeodomain gene Islet-1 (ISL1) encodes a transcription factor that has been associated with the multipotency of human cardiac progenitors, and in mice enables the correct deployment of second heart field (SHF) cells to become the myocardium of atria, right ventricle and outflow tract. Other markers have been identified that characterize subdomains of the SHF, such as the fibroblast growth factor Fgf10 in its anterior region. While functional evidence of its essential contribution has been demonstrated in many vertebrate species, SHF expression of Isl1 has been shown in only some models. We examined the relationship between human ISL1 and FGF10 within the embryonic time window during which the linear heart tube remodels into four chambers. ISL1 transcription demarcated an anatomical region supporting the conserved existence of a SHF in humans, and transcription factors of the GATA family were co-expressed therein. In conjunction, we identified a novel enhancer containing a highly conserved ISL1 consensus binding site within the FGF10 first intron. ChIP and EMSA demonstrated its direct occupation by ISL1. Transcription mediated by ISL1 from this FGF10 intronic element was enhanced by the presence of GATA4 and TBX20 cardiac transcription factors. Finally, transgenic mice confirmed that endogenous factors bound the human FGF10 intronic enhancer to drive reporter expression in the developing cardiac outflow tract. These findings highlight the interest of examining developmental regulatory networks directly in human tissues, when possible, to assess candidate non-coding regions that may be responsible for congenital malformations

Molecular Genetic Studies of ALSG, Kostmann Syndrome and a Novel Chromosome 10 Inversion

In summary, this thesis presents the localisation and identification of genetic variants of which some are disease associated and some considered to be neutral. Knowledge of the basic mechanisms behind human disorders is important both from a biological and medical point of view. The thesis is based on four papers of which the first two clarify the genetic basis of autosomal dominant aplasia of lacrimal and salivary glands (ALSG). ALSG is a rare disorder with high penetrance and variable expressivity characterized by dry mouth and eyes. In paper I, we located the ALSG gene to a 22 centiMorgan region on chromosome 5 through a genome-wide linkage scan with microsatellite markers in two families. Mutations were found in the gene encoding fibroblast growth factor 10 (FGF10) situated in the linked chromosome 5 region. Mice having only one copy of the FGF10 gene (Fgf10+/- mice) have a phenotype similar to ALSG, providing an animal model for the disorder. In paper II, we describe two additional patients with ALSG and missense mutations in FGF10, providing further genotype-phenotype correlations. The aim of paper III was to identify a gene involved in autosomal recessive severe congenital neutropenia (SCN), also referred to as Kostmann syndrome. The disease is characterized by a very low absolute neutrophil count and recurrent bacterial infections. Affected individuals from the family with SCN originally described by Dr Kostmann were genotyped with whole-genome SNP arrays. Autozygosity mapping identified a shared haplotype spanning 1.2 Mb on chromosome 1q22. This region contained 37 known genes, of which several were associated with myelopoiesis. Our finding contributed to the identification of the gene mutated in Kostmann syndrome. In paper IV a cytogenetic inversion on chromosome 10 was mapped and characterized. Sequence- and haplotype analysis of carriers from four non-related Swedish families revealed identical inversion breakpoints and established that the rearrangement was identical by descent. A retrospective study of karyotypes together with screening of large sample sets established that the inversion is a rare and inherited chromosome variant with a broad geographical distribution in Sweden. No consistent phenotype was found associated with the inversion. Genetic research increases the understanding of our genomes and makes it possible to discover variants contributing to disease. Identification of such genetic variants further enables studies of gene function and pathogenesis. The finding of the disease associated variants in this thesis will eventually contribute to improved diagnosis, prognosis, risk assessment and a future treatment of patients