Browsing by Subject "nutrients"

Cladocerans play a key role in the aquatic ecosystem. They are abundant in lakes and are an essential part in the carbon and energy transfer of the food webs. These species are, however, prone to various environmental changes. Estimates have shown that dissolved organic carbon (DOC) concentrations in northern lakes are likely to increase in the future. This increase of DOC in lakes has multiple impacts ranging from nutrient levels to shading impacts reducing primary productions. Investigating changes in cladocerans along a DOC gradient could help us understand how these species might develop in the future in our changing climate. In this Master’s Thesis, I studied how the cladoceran body length and community structure varied between 9 lakes with dissolved organic carbon (DOC) concentration ranging from 2.4-33.5 mg l-1. For the analyses, these lakes where divided into two groups with a threshold of 12 mg l-1 or into groups of three based on their DOC concentrations. Then, the results were compared with cladoceran length data from an earlier study. Additionally, the changes in phytoplankton abundances and communities as well as the relation between DOC concentration and other environmental variables were analysed. The results showed an increase in the cladoceran body length above the DOC threshold. Moreover, the changes in body length varied between the studied genera. Both Ceriodaphnia sp. and Diaphanosoma sp. body length decreased in groups with higher DOC concentrations while Bosmina sp. were larger at high DOC concentrations. DOC concentration did not have any significant effect on the community structure of zooplankton. The studied lakes varied from their environmental condition making comparisons and general statements challenging. The results indicated that DOC concentration regulates the planktonic communities, but it is solely an imprecise predictor for changes in zooplankton communities. However, cladoceran densities seemed to benefit from increased DOC concentrations as nutrient levels also increased. Changes in cladoceran body lengths were challenging to interpret, because there are multiple factors that can have an impact both alone and combined with others.

Tiivistelmä — Referat — Abstract Intestine renews itself from intestinal stem cells (ISCs) in response to cell damage and disease. Damaged and dead cells are replaced by ISCs through cell division followed by daughter cell differentiation. Disturbances in this process can lead to diseases such as cancer. Hexosamine biosynthetic pathway (HBP) is a mediator of systemic insulin signaling induced ISC proliferation. However, the full molecular mechanism of HBP mediated ISC proliferation is yet to be discovered. Deciphering the mechanisms of the regulation responsible for ISC renewal could pave way for disease etiology dependent on the rate of ISCs proliferation. In this project I use Drosophila genetic tools to elucidate transcriptional and translational level control of HBP regulated ISC proliferation. Glutamine Fructose-6-phosphate Amidotransferase (GFAT) activity limits the rate of N-Acetylglucosamine GlcNAc and consequently ISC proliferation. Thus, gfat2Δ1 mutant flies are used to study molecular regulation of HBP. Full midguts of Drosophila will be imaged using Aurox Clarity Spinning-disc Confocal system. Confocal 3D images will be analyzed using an image analysis software called linear analysis of midgut (LAM) to retain region specific data. Exploring ISC proliferation in relation to nutrient sensing pathways in the full midgut level is still novel and LAM provides region specific data in previously unprecedented detail. The end product of HBP pathway Uridine diphosphate N-acetylglucosamine (UDP-GlcNAc) was supplemented within the diet of the flies to observe its effect to the gfat2Δ1 ISC phenotype. UDP-GlcNac did not rescue the gfat2Δ1 ISCs. Usage of Drosophila genetic tools elucidated previously unknown transcriptional level regulation of HBP induced ISC proliferation: ATF4 knockdown in gfat2Δ1 mutant ISCs rescued gfat2Δ1 attenuated ISC division. In addition, ATF4 was indicated to possibly regulate the gfat2Δ1 phenotype via the regulation of growth through ribosome biogenesis and 4EBP translation inhibition. This study revealed the mediator of HBP, the transcription factor ATF4 to be the modulator of ISC proliferation.