Evidence against essential roles for subdomain 1 of actin in actomyosin sliding movements

We have engineered acto-S1chimera proteins carrying the entire actin inserted in loop 2 of the motor domain of Dictyostelium myosin II with 24 or 18 residue-linkers (CP24 and CP18, respectively). These proteins were capable of self-polymerization as well as copolymerization with skeletal actin and exhibited rigor-like structures. The MgATPase rate of CP24-skeletal actin copolymer was 1.06 s(-1), which is slightly less than the V(max) of Dictyostelium S1. Homopolymer filaments of skeletal actin, CP24, and CP18 moved at 4.7+/-0.6, 2.9+/-0.6, and 4.1+/-0.8 microm/s (mean+/-SD), respectively, on coverslips coated with skeletal myosin at 27 degrees C. Statistically thermodynamic considerations suggest that the S1 portion of chimera protein mostly resides on subdomain 1 (SD-1) of the actin portion even in the presence of ATP. This and the fact that filaments of CP18 with shorter linkers moved faster than CP24 filaments suggest that SD-1 might not be as essential as conventionally presumed for actomyosin sliding interactions.     

Salt sensitivity in chickpea is determined by sodium toxicity

Main conclusion

Salt sensitivity in chickpea is determined by Na⁺ toxicity, whereas relatively high leaf tissue concentrations of Cl^? were tolerated, and the osmotic component of 60-mM NaCl was not detrimental.Chickpea (Cicer arietinum L.) is sensitive to salinity. This study dissected the responses of chickpea to osmotic and ionic components (Na⁺ and/or Cl^?) of salt stress. Two genotypes with contrasting salt tolerances were exposed to osmotic treatments (?0.16 and ?0.29 MPa), Na⁺-salts, Cl^?-salts, or NaCl at 0, 30, or 60 mM for 42 days and growth, tissue ion concentrations and leaf gas-exchange were assessed. The osmotic treatments and Cl^?-salts did not affect growth, whereas Na⁺-salts and NaCl treatments equally impaired growth in either genotype. Shoot Na⁺ and Cl^? concentrations had markedly increased, whereas shoot K⁺ had declined in the NaCl treatments, but both genotypes had similar shoot concentrations of each of these individual ions after 14 and 28 days of treatments. Genesis836 achieved higher net photosynthetic rate (64–84 % of control) compared with Rupali (35–56 % of control) at equivalent leaf Na⁺ concentrations. We conclude that (1) salt sensitivity in chickpea is determined by Na⁺ toxicity, and (2) the two contrasting genotypes appear to differ in ‘tissue tolerance’ of high Na⁺. This study provides a basis for focus on Na⁺ tolerance traits for future varietal improvement programs for salinity tolerance in chickpea.

     

<Emphasis Type="Bold">Zinc nutrition in wheat-based cropping systems</Emphasis>

Background

Zinc (Zn) deficiency is one of the most important micronutrient disorders affecting human health. Wheat is the staple food for 35% of the world’s population and is inherently low in Zn, which increases the incidence of Zn deficiency in humans. Major wheat-based cropping systems viz. rice–wheat, cotton–wheat and maize–wheat are prone to Zn deficiency due to the high Zn demand of these crops.

Methods

This review highlights the role of Zn in plant biology and its effect on wheat-based cropping systems. Agronomic, breeding and molecular approaches to improve Zn nutrition and biofortification of wheat grain are discussed.

Results

Zinc is most often applied to crops through soil and foliar methods. The application of Zn through seed treatments has improved grain yield and grain Zn status in wheat. In cropping systems where legumes are cultivated in rotation with wheat, microorganisms can improve the available Zn pool in soil for the wheat crop. Breeding and molecular approaches have been used to develop wheat genotypes with high grain Zn density.

Conclusions

Options for improving grain yield and grain Zn concentration in wheat include screening wheat genotypes for higher root Zn uptake and grain translocation efficiency, the inclusion of these Zn-efficient genotypes in breeding programs, and Zn fertilization through soil, foliar and seed treatments.

     

Adaptation to Stochastic Temporal Variations in Intratumoral Blood Flow: The Warburg Effect as a Bet Hedging Strategy

While most cancers promote ingrowth of host blood vessels, the resulting vascular network usually fails to develop a mature organization, resulting in abnormal vascular dynamics with stochastic variations that include slowing, cessation, and even reversal of flow. Thus, substantial spatial and temporal variations in oxygen concentration are commonly observed in most cancers. Cancer cells, like all living systems, are subject to Darwinian dynamics such that their survival and proliferation are dependent on developing optimal phenotypic adaptations to local environmental conditions. Here, we consider the environmental stresses placed on tumors subject to profound, frequent, but stochastic variations in oxygen concentration as a result of temporal variations in blood flow. While vascular fluctuations will undoubtedly affect local concentrations of a wide range of molecules including growth factors (e.g., estrogen), substrate (oxygen, glucose, etc.), and metabolites (\(\hbox {H}^{+})\), we focus on the selection forces that result solely from stochastic fluctuations in oxygen concentration. The glucose metabolism of cancer cells has been investigated for decades following observations that malignant cells ferment glucose regardless of oxygen concentration, a condition termed the Warburg effect. In contrast, normal cells cease fermentation under aerobic conditions and this physiological response is termed the Pasteur effect. Fermentation is markedly inefficient compared to cellular respiration in terms of adenosine triphosphate (ATP) production, generating just 2 ATP/glucose, whereas respiration generates 38 ATP/glucose. This inefficiency requires cancer cells to increase glycolytic flux, which subsequently increases acid production and can significantly acidify local tissue. Hence, it initially appears that cancer cells adopt a disadvantageous metabolic phenotype. Indeed, this metabolic “hallmark” of cancer is termed “energy dysregulation.” However, if cancers arise through an evolutionary optimization process, any common observed property must confer an adaptive advantage. In the present work, we investigate the hypothesis that aerobic glycolysis represents an adaptation to stochastic variations in oxygen concentration stemming from disordered intratumoral blood flow. Using mathematical models, we demonstrate that the Warburg effect evolves as a conservative metabolic bet hedging strategy in response to stochastic fluctuations of oxygen. Specifically, the Warburg effect sacrifices fitness in physoxia by diverting resources from the more efficient process of respiration, but preemptively adapts cells to hypoxia because fermentation produces ATP anaerobically. An environment with sufficiently stochastic fluctuations of oxygen will select for the bet hedging (Warburg) phenotype since it is modestly successful irrespective of oxygen concentration.