Anthranilate fluorescence marks a calcium-propagated necrotic wave that promotes organismal death in C. elegans.

For cells the passage from life to death can involve a regulated, programmed transition. In contrast to cell death, the mechanisms of systemic collapse underlying organismal death remain poorly understood. Here we present evidence of a cascade of cell death involving the calpain-cathepsin necrosis pathway that can drive organismal death in Caenorhabditis elegans. We report that organismal death is accompanied by a burst of intense blue fluorescence, generated within intestinal cells by the necrotic cell death pathway. Such death fluorescence marks an anterior to posterior wave of intestinal cell death that is accompanied by cytosolic acidosis. This wave is propagated via the innexin INX-16, likely by calcium influx. Notably, inhibition of systemic necrosis can delay stress-induced death. We also identify the source of the blue fluorescence, initially present in intestinal lysosome-related organelles (gut granules), as anthranilic acid glucosyl esters--not, as previously surmised, the damage product lipofuscin. Anthranilic acid is derived from tryptophan by action of the kynurenine pathway. These findings reveal a central mechanism of organismal death in C. elegans that is related to necrotic propagation in mammals--e.g., in excitotoxicity and ischemia-induced neurodegeneration. Endogenous anthranilate fluorescence renders visible the spatio-temporal dynamics of C. elegans organismal death.

QTL analysis for sugar-regulated leaf senescence supports flowering-dependent and -independent senescence pathways.

*The aim of this work was to determine the genetic basis of sugar-regulated senescence and to explore the relationship with other traits, including flowering and nitrogen-use efficiency. *Quantitative trait loci (QTLs) for senescence were mapped in the Arabidopsis Bay-0 x Shahdara recombinant-inbred line (RIL) population after growth on glucose-containing medium, which accelerates senescence. The extent of whole-rosette senescence was determined by imaging the maximum quantum yield of photosystem II (F(v)/F(m)). *A major QTL on the top of chromosome 4 colocalized with FRI, a major determinant of flowering. This QTL interacted epistatically with a QTL on chromosome 5, where the floral repressor FLC localizes. Vernalization accelerated senescence in late-flowering lines with functional FRI and FLC alleles. Comparison with previous results using the Bay-0 x Shahdara population showed that rapid rosette senescence on glucose-containing medium was correlated with early flowering and high sugar content in compost-grown plants. In addition, correlation was found between the expression of flowering and senescence-associated genes in Arabidopsis accessions. However, an additional QTL on chromosome 3 was not linked to flowering, but to nitrogen-use efficiency. *The results show that whole-rosette senescence is genetically linked to the vernalization-dependent control of flowering, but is also controlled by flowering-independent pathways.

Motivational change in an inpatient anorexia nervosa population and implications for treatment.

OBJECTIVE: The relationship between motivation and recovery in anorexia nervosa has received increased attention in the research literature although few controlled investigations of increasing motivation in this population exist. Three questions were therefore examined in an inpatient anorexia nervosa population: (i) does baseline motivation predict change in eating pathology; (ii) does change in motivation predict change in eating pathology; and (iii) can we increase motivation to recover in this group? METHOD: Inpatients (n=47) in a specialist weight disorder unit with a mean age of 21.85 years (SD=5.37) were randomly allocated to receive four sessions of motivational interviewing with a novice therapist in addition to treatment as usual (n=22) or treatment as usual alone (n=25). Assessment of eating pathology and motivation to recover was conducted on three occasions: at admission (baseline), and at 2- and 6 week follow up. Eating pathology was assessed using the Eating Disorder Examination and self-reported motivation was assessed using the Anorexia Nervosa Stages of Change Questionnaire and six Likert scales. RESULTS: Higher baseline motivation across five of the seven measures predicted significant decreases in eating pathology, and increased Anorexia Nervosa Stages of Change Questionnaire scores between baseline and 2 week follow up predicted significant improvement in eating pathology between baseline and 6 week follow up. Significantly more patients were lost to follow up from the treatment as usual compared to the motivational interviewing group. More patients in the motivational interviewing condition moved from low readiness to change at baseline to high readiness to change at 2 and 6 week follow up. CONCLUSIONS: Motivation is an important predictor of change in anorexia nervosa and preliminary evidence is provided that motivation can be improved in this population. Further investigations, however, of ways of improving motivation in this population need to be conducted, along with the impact of motivational changes on treatment outcome.