48 research outputs found

    Differences in bud burst timing and bud freezing tolerance among interior and coastal seed sources of Douglas fir

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    The need for species that will grow well through ongoing climate change has increased the interest in Douglas fir [Pseudotsuga menziesii (Mirb.) Franco] in Sweden. One of the most common problems seen in plantations of Douglas fir seedlings is damage caused by late spring frost, known to be highly correlated with the timing of bud burst. The objective of this study was to investigate spring-related bud development under Nordic conditions of seven Douglas fir provenances and to compare data with a local provenance of Norway spruce (Picea abies (L.) Karst). Results from a field trial and a greenhouse-based study were compared. The interior Douglas fir provenances exhibited an earlier bud burst than coastal provenances, both in the greenhouse and in the field trial. When comparing differences within the groups of interior and coastal Douglas fir provenances, no differences could be found. The local Norway spruce, only grown in the greenhouse, showed an intermediate bud development profile similar to the interior Douglas fir provenance Three Valley. We therefore suggest that Three Valley could be planted at the same locations as the investigated local provenance of Norway spruce in mid-Sweden. To avoid spring frost damage the Douglas fir seedlings need to be frozen stored and planted late in spring. Planting under shelterwood can also help protect the seedlings from spring frost damages. As similar results for bud development patterns of Douglas fir and Norway spruce provenances were obtained from the greenhouse and field trials, greenhouse tests could facilitate selection of provenances

    Inhibition of AMPK activity in response to insulin in adipocytes : involvement of AMPK pS485, PDEs, and cellular energy levels

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    Insulin resistance in obesity and type 2 diabetes has been shown to be associated with decreased de novo fatty acid (FA) synthesis in adipose tissue. It is known that insulin can acutely stimulate FA synthesis in adipocytes; however, the mechanisms underlying this effect are unclear. The rate-limiting step in FA synthesis is catalyzed by acetyl-CoA carboxylase (ACC), known to be regulated through inhibitory phosphorylation at S79 by the AMP-activated protein kinase (AMPK). Previous results from our laboratory showed an inhibition of AMPK activity by insulin, which was accompanied by PKB-dependent phosphorylation of AMPK at S485. However, whether the S485 phosphorylation is required for insulin-induced inhibition of AMPK or other mechanisms underlie the reduced kinase activity is not known. To investigate this, primary rat adipocytes were transduced with a recombinant adenovirus encoding AMPK-WT or a nonphosphorylatable AMPK S485A mutant. AMPK activity measurements by Western blot analysis and in vitro kinase assay revealed that WT and S485A AMPK were inhibited to a similar degree by insulin, indicating that AMPK S485 phosphorylation is not required for insulin-induced AMPK inhibition. Further analysis suggested an involvement of decreased AMP-to-ATP ratios in the insulin-induced inhibition of AMPK activity, whereas a possible contribution of phosphodiesterases was excluded. Furthermore, we show that insulin-induced AMPK S485 phosphorylation also occurs in human adipocytes, suggesting it to be of an importance yet to be revealed. Altogether, this study increases our understanding of how insulin regulates AMPK activity, and with that, FA synthesis, in adipose tissue
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