1,168 research outputs found
Geochemistry and identification of Australian red ochre deposits
Between 1994 and 1998 the authors undertook a project to look at the feasibility of
using geochemical signatures to identify the sources of ochres recovered in
archaeological excavations. This research was supported by AIATSIS research grants
G94/4879, G96/5222 and G98/6143.The two substantive reports on this research
(listed below) have remained unpublished until now and are brought together in this
Palaeoworks Technical Paper to make them more generally accessible to students
and other researchers.
Smith, M. A. and B. Fankhauser (1996) An archaeological perspective on the
geochemistry of Australian red ochre deposits: Prospects for fingerprinting
major sources. A report to the Australian Institute of Aboriginal and Torres
Strait Islander Studies, Canberra.
Smith, M. A. and B. Fankhauser (2003) G96/5222 - Further characterisation
and sourcing of archaeological ochres. A report to the Australian Institute of
Aboriginal and Torres Strait Islander Studies, Canberra
Conditional Involvement of CONSTITUTIVE PHOTOMORPHOGENIC1 in the Degradation of Phytochrome A.
All higher plants possess multiple phytochrome photoreceptors, with phytochrome A (phyA) being light labile and other members of the family being relatively light stable (phyB-phyE in Arabidopsis [Arabidopsis thaliana]). phyA also differs from other members of the family because it enables plants to deetiolate in far-red light-rich environments typical of dense vegetational cover. Later in development, phyA counteracts the shade avoidance syndrome. Light-induced degradation of phyA favors the establishment of a robust shade avoidance syndrome and was proposed to be important for phyA-mediated deetiolation in far-red light. phyA is ubiquitylated and targeted for proteasome-mediated degradation in response to light. Cullin1 and the ubiquitin E3 ligase CONSTITUTIVE PHOTOMORPHOGENIC1 (COP1) have been implicated in this process. Here, we systematically analyze the requirement of cullins in this process and show that only CULLIN1 plays an important role in light-induced phyA degradation. In addition, the role of COP1 in this process is conditional and depends on the presence of metabolizable sugar in the growth medium. COP1 acts with SUPPRESSOR OF PHYTOCHROME A (SPA) proteins. Unexpectedly, the light-induced decline of phyA levels is reduced in spa mutants irrespective of the growth medium, suggesting a COP1-independent role for SPA proteins
Contrasting growth responses in lamina and petiole during neighbor detection depend on differential auxin responsiveness rather than different auxin levels.
Foliar shade triggers rapid growth of specific structures that facilitate access of the plant to direct sunlight. In leaves of many plant species, this growth response is complex because, although shade triggers the elongation of petioles, it reduces the growth of the lamina. How the same external cue leads to these contrasting growth responses in different parts of the leaf is not understood. Using mutant analysis, pharmacological treatment and gene expression analyses, we investigated the role of PHYTOCHROME INTERACTING FACTOR7 (PIF7) and the growth-promoting hormone auxin in these contrasting leaf growth responses. Both petiole elongation and lamina growth reduction are dependent on PIF7. The induction of auxin production is both necessary and sufficient to induce opposite growth responses in petioles vs lamina. However, these contrasting growth responses are not caused by different auxin concentrations in the two leaf parts. Our work suggests that a transient increase in auxin levels triggers tissue-specific growth responses in different leaf parts. We provide evidence suggesting that this may be caused by the different sensitivity to auxin in the petiole vs the blade and by tissue-specific gene expression
Increased activity of the first two enzymes of tryptophan biosynthesis
Increased activity of the first two enzymes of tryptophan biosynthesi
Phototropin-mediated perception of light direction in leaves regulates blade flattening.
One conserved feature among angiosperms is the development of flat thin leaves. This developmental pattern optimizes light capture and gas exchange. The blue light (BL) receptors phototropins are required for leaf flattening, with the null phot1phot2 mutant showing curled leaves in Arabidopsis (Arabidopsis thaliana). However, key aspects of their function in leaf development remain unknown. Here, we performed a detailed spatiotemporal characterization of phototropin function in Arabidopsis leaves. We found that phototropins perceive light direction in the blade, and, similar to their role in hypocotyls, they control the spatial pattern of auxin signaling, possibly modulating auxin transport, to ultimately regulate cell expansion. Phototropin signaling components in the leaf partially differ from hypocotyls. Moreover, the light response on the upper and lower sides of the leaf blade suggests a partially distinct requirement of phototropin signaling components on each side. In particular, NON PHOTOTROPIC HYPOCOTYL 3 showed an adaxial-specific function. In addition, we show a prominent role of PHYTOCHROME KINASE SUBSTRATE 3 in leaf flattening. Among auxin transporters, PIN-FORMED 3,4,7 and AUXIN RESISTANT 1 (AUX1)/LIKE AUXIN RESISTANT 1 (LAX1) are required for the response while ABCB19 has a regulatory role. Overall, our results show that directional BL perception by phototropins is a key aspect of leaf development, integrating endogenous and exogenous signals
Light intensity modulates the regulatory network of the shade avoidance response in Arabidopsis.
Plants such as Arabidopsis thaliana respond to foliar shade and neighbors who may become competitors for light resources by elongation growth to secure access to unfiltered sunlight. Challenges faced during this shade avoidance response (SAR) are different under a light-absorbing canopy and during neighbor detection where light remains abundant. In both situations, elongation growth depends on auxin and transcription factors of the phytochrome interacting factor (PIF) class. Using a computational modeling approach to study the SAR regulatory network, we identify and experimentally validate a previously unidentified role for long hypocotyl in far red 1, a negative regulator of the PIFs. Moreover, we find that during neighbor detection, growth is promoted primarily by the production of auxin. In contrast, in true shade, the system operates with less auxin but with an increased sensitivity to the hormonal signal. Our data suggest that this latter signal is less robust, which may reflect a cost-to-robustness tradeoff, a system trait long recognized by engineers and forming the basis of information theory
Controlling Size in Multicellular Organs: Focus on the Leaf
In leaves, cells get larger as cell division decreases or the ploidy increases. This might seem a logical response, but the controls are more complicated
Nuclear phytochrome a signaling promotes phototropism in Arabidopsis.
Phototropin photoreceptors (phot1 and phot2 in Arabidopsis thaliana) enable responses to directional light cues (e.g., positive phototropism in the hypocotyl). In Arabidopsis, phot1 is essential for phototropism in response to low light, a response that is also modulated by phytochrome A (phyA), representing a classical example of photoreceptor coaction. The molecular mechanisms underlying promotion of phototropism by phyA remain unclear. Most phyA responses require nuclear accumulation of the photoreceptor, but interestingly, it has been proposed that cytosolic phyA promotes phototropism. By comparing the kinetics of phototropism in seedlings with different subcellular localizations of phyA, we show that nuclear phyA accelerates the phototropic response, whereas in the fhy1 fhl mutant, in which phyA remains in the cytosol, phototropic bending is slower than in the wild type. Consistent with this data, we find that transcription factors needed for full phyA responses are needed for normal phototropism. Moreover, we show that phyA is the primary photoreceptor promoting the expression of phototropism regulators in low light (e.g., PHYTOCHROME KINASE SUBSTRATE1 [PKS1] and ROOT PHOTO TROPISM2 [RPT2]). Although phyA remains cytosolic in fhy1 fhl, induction of PKS1 and RPT2 expression still occurs in fhy1 fhl, indicating that a low level of nuclear phyA signaling is still present in fhy1 fhl
Adverse perinatal outcomes for obese women are influenced by the presence of comorbid diabetes and hypertensive disorders
Maternal obesity often occurs together with comorbid diabetes and hypertensive disorders. All three conditions are independently associated with negative perinatal outcomes. Our objective was to determine the risk and burden of adverse perinatal outcome that could be attributed to maternal obesity in combination with a comorbid status. We analyzed data from 324'664 singleton deliveries in Switzerland between 2005 and 2016. For the association of maternal obesity in the presence or absence of comorbidities with various perinatal outcomes, we estimated adjusted relative risk (RR) using multivariable regression modeling and determined the multivariable-adjusted attributable fraction of the population (AFp). Obesity was a main predictor for macrosomia, fracture of the clavicle, failure to progress in labor and prolonged labor. By stratifying women based on comorbidities, we identified significantly increased risk for preterm birth and early neonatal death only for women diagnosed with a comorbidity. However, various other outcomes were independently associated with either obesity or comorbidities. The AFp showed greatest reduction in comorbidities (15.4/15.0/13.2%), in macrosomia (6.3%) and in shoulder dystocia (4.8%) if all women were to become non-obese. We suggest that comorbidities such as diabetes and hypertensive disorders should be considered when relating maternal obesity to adverse perinatal outcomes
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