Rapid physiological adjustment of roots to localized soil enrichment

SOIL microsites rich in available nutrients are an important source of mineral nutrients for plants in many environments(1-5). Patchiness in nutrient availability below ground is analogous to resource availability in canopy gaps above ground(6). Although the physiological changes occurring in leaves exposed to sun and shade in canopy gaps are well known(7-9), we do not know any studies that show similar physiological changes in roots in enriched soil patches. Here we present evidence of large and rapid increases in the uptake kinetics of plant roots after creating nutrient-rich soil patches in the field. The mean rate of phosphate uptake at a given external phosphate concentration increased by as much as 80% for roots from enriched soil patches compared with roots of control patches treated with distilled water. The changes took place within days of patch treatment. This degree of plasticity was particularly notable for plants growing in soils of very low available phosphorus. These results showing rapid physiological plasticity of roots in fertile soil microsites have important implications for the theory and modelling of nutrient uptake in all soils.     

Why endophenotype development requires families

Endophenotypes are heritable quantitative traits that are associated with disease liability, can be measured in both affected and unaffected individuals, and provide much greater power to localize and identify risk genes for mental illness than does affection status alone. Traditionally, endophenotypic markers for psychiatric illnesses include in vivo neuroanatomic and functional magnetic resonance imaging measurements and indices of neurocognitive abilities. However, neurocognitive and neuroimaging measure...     

BOOK REVIEWS: Partnership and Participation by Ann Taket and Leroy White. Sustainable Development: Economics and Policy by P. K. Rao.

Systemic Practice and Action Research -     

非正式支持与心理健康的三大来源:中美老人比较

研究调查中美老年人三大非正式支持--家庭、朋友和邻里,以及心理健康--自尊、抑郁和孤独的来源.研究结果发现:家庭的支持是美国老年人的健康最期望来源,而在中国则为邻里与朋友的支持.     

Non-canonical activation of Notch signaling/target genes in vertebrates

Evolutionarily conserved Notch signaling orchestrates diverse physiological mechanisms during metazoan development and homeostasis. Classically, ligand-activated Notch receptors transduce the signaling cascade through the interaction of DNA-bound CBF1-co-repressor complex. However, recent reports have demonstrated execution of a CBF1-independent Notch pathway through signaling cross-talks in various cells/tissues. Here, we have tried to congregate the reports that describe the non-canonical/CBF1-independent Notch signaling and target gene activation in vertebrates with specific emphasis on their functional relevance.     

Francesco Patrizi da Cherso's concept of space and its later influence

This study considers the contribution of Francesco Patrizi da Cherso (1529–1597) to the development of the concepts of void space and an infinite universe. Patrizi plays a greater role in the development of these concepts than any other single figure in the sixteenth century, and yet his work has been almost totally overlooked. I have outlined his views on space in terms of two major aspects of his philosophical attitude: on the one hand, he was a devoted Platonist and sought always to establish Platonism, albeit his own version of it, as the only currect philosophy; and on the other hand, he was more determinedly anti-Aristotelian than any other philosopher at that time. Patrizi's concept of space has its beginnings in Platonic notions, but is extended and refined in the light of a vigorous critique of Aristotle's position. Finally, I consider the influence of Patrizi's ideas in the seventeenth century, when various thinkers are seeking to overthrow the Aristotelian concept of place and the equivalence of dimensionality with corporeality. Pierre Gassendi (1592–1652), for example, needed a coherent concept of void space in which his atoms could move, while Henry More (1614–1687) sought to demonstrate the reality of incorporeal entities by reference to an incorporeal space. Both men could find the arguments they needed in Patrizi's comprehensive treatment of the subject.     

The tyrosine phosphatase SHP-1 negatively regulates cytotrophoblast proliferation in first-trimester human placenta by modulating EGFR activation

Insulin-like growth factors (IGFs) influence placental cell (cytotrophoblast) kinetics. We recently reported that the protein tyrosine phosphatase (PTP) SHP-2 positively regulates IGF actions in the placenta. In other systems, the closely related PTP, SHP-1, functions as a negative regulator of signaling events but its role in the placenta is still unknown. We examined the hypothesis that SHP-1 negatively regulates IGF actions in the human placenta. Immunohistochemical (IHC) analysis demonstrated that SHP-1 is abundant in cytotrophoblast. SHP-1 expression was decreased in first-trimester placental explants using siRNA; knockdown did not alter IGF-induced proliferation but it significantly enhanced proliferation in serum-free conditions, revealing that placental growth is endogenously regulated. Candidate regulators were determined by using antibody arrays, Western blotting, and IHC to examine the activation status of multiple receptor tyrosine kinases (RTKs) in SHP-1-depleted explants; amongst the alterations observed was enhanced activation of EGFR, suggesting that SHP-1 may interact with EGFR to inhibit proliferation. The EGFR tyrosine kinase inhibitor PD153035 reversed the elevated proliferation seen in the absence of SHP-1. This study demonstrates a role for SHP-1 in human trophoblast turnover and establishes SHP-1 as a negative regulator of EGFR activation. Targeting placental SHP-1 expression may provide therapeutic benefits in common pregnancy conditions with abnormal trophoblast proliferation.     

Alkyltransferase-like proteins: molecular switches between DNA repair pathways

Alkyltransferase-like proteins (ATLs) play a role in the protection of cells from the biological effects of DNA alkylation damage. Although ATLs share functional motifs with the DNA repair protein and cancer chemotherapy target O ⁶-alkylguanine-DNA alkyltransferase, they lack the reactive cysteine residue required for alkyltransferase activity, so its mechanism for cell protection was previously unknown. Here we review recent advances in unraveling the enigmatic cellular protection provided by ATLs against the deleterious effects of DNA alkylation damage. We discuss exciting new evidence that ATLs aid in the repair of DNA O ⁶-alkylguanine lesions through a novel repair cross-talk between DNA-alkylation base damage responses and the DNA nucleotide excision repair pathway.