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The high Arctic is the world's fasting warming biome, allowing access to sections of previously inaccessible land for resource extraction. Starting in 2011, exploration of one of the Earth's largest undeveloped coal seams was initiated in a relatively pristine, polar desert environment in the Canadian high Arctic. Due to the relative lack of historic anthropogenic disturbance, significant gaps in knowledge exist on how the landscape will be impacted by development., At an abandoned airstrip located near the area of current exploration, we used a disturbance case-control approach to evaluate the long-term ecological consequences of high Arctic infrastructure disturbance to vegetation and sensitive, ice-rich permafrost. We quantified: (i) long-term effects on vegetation diversity, soil nutrients and abiotic ground conditions and (ii) the alteration of the ground surface topography and legacy of subsurface thermal changes., We found that in over 60 years since abandonment, the disturbed landscape has not recovered to initial conditions but instead reflects a disturbance-initiated succession towards a different stable-state community., Microtopography greatly influenced recovery patterns in the landscape. The terrain overlaying buried ice (ice-wedge polygon troughs) was the most sensitive to disturbance and had a different species composition, decreased plot-level species richness, significant increases in vegetation cover and a drastically reduced seasonal fluctuation in subsurface temperatures. In contrast, disturbed polygon tops showed resiliency in vegetation recovery, but still had remarkable increases in depth of seasonal soil thaw (active layer)., Synthesis and applications. Our results indicate that disturbance effects differ depending on microtopographic features, leading to an increased patchiness of the landscape as found elsewhere in the Arctic. Managers who wish to lessen their impact on high Arctic environments should avoid areas of sensitive, ice-rich permafrost, constrain the geographic scale of near-surface ground disturbance, limit vegetation removal where possible and reseed disturbed areas with native species. [ABSTRACT FROM AUTHOR]

Hematopoietic stem cells (HSCs) originate within the aortic-gonado-mesonephros (AGM) region of the midgestation embryo, but the cell type responsible for their emergence is unknown since critical hematopoietic factors are expressed in both the AGM endothelium and its underlying mesenchyme. Here we employ a temporally restricted genetic tracing strategy to selectively label the endothelium, and separately its underlying mesenchyme, during AGM development. Lineage tracing endothelium, via an inducible VE-cadherin Cre line, reveals that the endothelium is capable of HSC emergence. The endothelial progeny migrate to the fetal liver, and later to the bone marrow, and are capable of expansion, self- renewal, and multilineage hematopoietic differentiation. HSC capacity is exclusively endothelial, as ex vivo analyses demonstrate lack of VE-cadherin Cre induction in circulating and fetal liver hematopoietic populations. Moreover, AGM mesenchyme, as selectively traced via a myocardin Cre line, is incapable of hematopoiesis. Our genetic tracing strategy therefore reveals an endothelial origin of HSCs. [ABSTRACT FROM AUTHOR]

Maintenance of single-layered endothelium, squamous endothelial cell shape, and formation of a patent vascular lumen all require defined endothelial cell polarity. Loss of beta1 integrin (Itgb1) in nascent endothelium leads to disruption of arterial endothelial cell polarity and lumen formation. The loss of polarity is manifested as cuboidal-shaped endothelial cells with dysregulated levels and mislocalization of normally polarized cell-cell adhesion molecules, as well as decreased expression of the polarity gene Par3 (pard3). beta1 integrin and Par3 are both localized to the endothelial layer, with preferential expression of Par3 in arterial endothelium. Luminal occlusion is also exclusively noted in arteries, and is partially rescued by replacement of Par3 protein in beta1-deficient vessels. Combined, our findings demonstrate that beta1 integrin functions upstream of Par3 as part of a molecular cascade required for endothelial cell polarity and lumen formation., ((c) 2010 Elsevier Inc. All rights reserved.)