1997 research outputs found
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Beaver-Dredged Canals and their Spacial Relationship to Beaver-Cut Stumps
Get PDFCastor canadensis Kuhl (North American beavers) are central place foragers whocollect woody plants and building materials from their surroundings and return to a main body of water containing a lodge or food cache. It has been suggested that beavers dredge water-filled canals to extend access to foraging areas; however, the possibility that these engineered transportation routes function as extensions to the beavers\u27 central place has yet to be considered. Our objective in this study was to gain a better understanding of the formation and utilization of canals by beavers and thus further elucidate the complex foraging behavior of these ecosystem engineers. During 2004–2011, we mapped beaver ponds, canals, and cut stumps in eight groundwater-fed wetlands, from at least four separate colonies, in Indianapolis, IN. We found that the mean length, depth, and width of the beaver-dredged canals were 604.3 6 493.1 m, 28.0 6 22.2 cm, and 107.7 6 107.1 cm respectively. Two of the canal systems were mapped for multiple years and their length, depth, and width increased over time and supported the prediction that beavers continuously engineer these canal systems to extend their foraging area into new locations. In addition, and in contrast to previous studies, we found that the number of beaver-cut stumps was negatively related to distance from canals, but not from the body of water containing their lodges. We recommend that studies of optimal foraging in beavers take canals into account, where applicable, when relating foraging to distance from the central place
Characterization of NOL7 gene point mutations, promoter methylation, and protein expression in cervical cancer.
No full textNOL7 is a putative tumor suppressor gene localized to 6p23, a region with frequent loss of heterozygosity in a number of cancers, including cervical cancer (CC). We have previously demonstrated that reintroduction of NOL7 into CC cells altered the angiogenic phenotype and suppressed tumor growth in vivo by 95%. Therefore, to understand its mechanism of inactivation in CC, we investigated the genetic and epigenetic regulation of NOL7. NOL7 mRNA and protein levels were assessed in 13 CC cell lines and 23 consecutive CC specimens by real-time quantitative polymerase chain reaction, western blotting, and immunohistochemistry. Methylation of the NOL7 promoter was analyzed by bisulfite sequencing and mutations were identified through direct sequencing. A CpG island with multiple CpG dinucleotides spanned the 5\u27 untranslated region and first exon of NOL7. However, bisulfite sequencing failed to identify persistent sites of methylation. Mutational sequencing revealed that 40% of the CC specimens and 31% of the CC cell lines harbored somatic mutations that may affect the in vivo function of NOL7. Endogenous NOL7 mRNA and protein expression in CC cell lines were significantly decreased in 46% of the CC cell lines. Finally, immunohistochemistry demonstrated strong NOL7 nucleolar staining in normal tissues that decreased with histologic progression toward CC. NOL7 is inactivated in CC in accordance with the Knudson 2-hit hypothesis through loss of heterozygosity and mutation. Together with evidence of its in vivo tumor suppression, these data support the hypothesis that NOL7 is the legitimate tumor suppressor gene located on 6p23
BMP3 Suppresses Osteoblast Differentiation of Bone Marrow Stromal Cells Via Interaction With Acvr2b.
Get PDFEnhancing bone morphogenetic protein (BMP) signaling increases bone formation in a variety of settings that target bone repair. However, the role of BMP in the maintenance of adult bone mass is not well understood. Targeted disruption of BMP3 in mice results in increased trabecular bone formation, whereas transgenic overexpression of BMP3 in skeletal cells leads to spontaneous fracture, consistent with BMP3 having a negative role in bone mass regulation. Here we investigate the importance of BMP3 as a mediator of BMP signaling in the adult skeleton. We find that osteoblasts (OBL) and osteocytes are the source of BMP3 in adult bone. Using in vitro cultures of primary bone marrow stromal cells, we show that overexpression of BMP3 suppresses OBL differentiation, whereas loss of BMP3 increases colony-forming unit fibroblasts and colony-forming unit OBL. The ability of BMP3 to affect OBL differentiation is due to its interaction with activin receptor type 2b (Acvr2b) because knockdown of endogenous Acvr2b in bone marrow stromal cells reduces the suppressive effect of BMP3 on OBL differentiation. These findings best fit a model in which BMP3, produced by mature bone cells, acts to reduce BMP signaling through Acvr2b in skeletal progenitor cells, limiting their differentiation to mature OBL. Our data further support the idea that endogenous BMPs have a physiological role in regulating adult bone mass
