The continuous flowering gene in rose is a floral inhibitor

In rose, RoKSN, a TFL1 homologue, is a key regulator of continuous flowering. To study the function of this gene in planta, protocols of plant transformation are needed. We complemented tfl1 Arabidopsis mutants and ectopically expressed RoKSN in a continuous-flowering rose. In Arabidopsis, RoKSN complemented the tfl1 mutant by rescuing late flowering and indeterminate growth. In continuous-flowering rose, the ectopic expression of RoKSN led to the absence of flowering. In these transgenic roses, a study of genes implied in the floral regulation was carried out. The floral activator transcripts decreased whereas the FD transcription factor is up-regulated. We conclude that RoKSN is a floral repressor and could regulate the expression of transcripts as RoFT and RoFD. These results could strengthen a mechanism of competitive interactions of RoFT and RoKSN with a common partner, FD to move towards flowering or vegetative developments

RoKSN, a floral repressor, forms protein complexes with RoFD and RoFT to regulate vegetative and reproductive development in rose

FT/TFL1 family members have been known to be involved in the development and flowering in plants. In rose, RoKSN, a TFL1 homologue, is a key regulator of flowering, whose absence causes continuous flowering. Our objectives are to functionally validate RoKSN and to explore its mode of action in rose.We complemented Arabidopsis tfl1 mutants and ectopically expressed RoKSN in a continuous-flowering (CF) rose. Using different protein interaction techniques, we studied RoKSN interactions with RoFD and RoFT and possible competition. In Arabidopsis, RoKSN complemented the tfl1 mutant by rescuing late flowering and indeterminate growth. In CF roses, the ectopic expression of RoKSN led to the absence of flowering. Different branching patterns were observed and some transgenic plants had an increased number of leaflets per leaf. In these transgenic roses, floral activator transcripts decreased. Furthermore, RoKSN was able to interact both with RoFD and the floral activator, RoFT. Protein interaction experiments revealed that RoKSN and RoFT could compete with RoFD for repression and activation of blooming, respectively. We conclude that RoKSN is a floral repressor and is also involved in the vegetative development of rose. RoKSN forms a complex with RoFD and could compete with RoFT for repression of flowering

Deciphering the genetic determinism of bud phenology in apple progenies: a new insight into chilling and heat requirement effects on flowering dates and positional candidate genes

The present study investigates the genetic determinism of bud phenological traits using two segregating F1 apple (Malus x domestica) progenies. Phenological trait variability was dissected into genetic and climatic components using mixed linear modeling, and estimated best linear unbiased predictors were used for quantitative trait locus (QTL) detection. For flowering dates, year effects were decomposed into chilling and heat requirements based on a previously developed model. QTL analysis permitted the identification of two major and population-specific genomic regions on LG08 and LG09. Both ‘chilling requirement’ and ‘heat requirement’ periods influenced flowering dates, although their relative impact was dependent on the genetic background. Using the apple genome sequence data, putative candidate genes underlying one major QTL were investigated. Numerous key genes involved in cell cycle control were identified in clusters within the confidence interval of the major QTL on LG09. Our results contribute towards a better understanding of the interaction between QTLs and climatic conditions, and provide a basis for the identification of genes involved in bud growth resumption

Characterization and localization of partial-discharge-induced pulses in fission chambers designed for sodium-cooled fast reactors

During the operation of the Superphenix and Phenix reactors, an aberrant electrical signal was detected from the fission chambers used for neutron flux monitoring. This signal, thought to be due to partial electrical discharge (PD) is similar to the signal resulting from neutron interactions, and is generated in fission chambers at temperatures above 400 °C. This paper reports work on the characterization and localization of the source of this electrical signal in a High Temperature Fission Chamber (HTFC). The relation between the shape of the PD signal and various parameters (nature and pressure of the chamber filling gas, electrode gap distance, and fission chamber geometry) are first described. Next, experiments designed to identify the location within the chambers where the PD are being generated are presented. After verification and refinement of the results of these localization studies, it should be possible to propose changes to the fission chamber in order to reduce or eliminate the PD signal

Autonomic nervous system control of the cardiovascular and respiratory systems in asthma

SummaryPatients with asthma have exaggerated bronchoconstriction of their airways in response to certain indirect (e.g. cold air, allergens, dust, exercise) or direct (e.g. inhaled methacholine) stimuli. This ‘hyper-reactivity’ usually co-exists with airway inflammation, although the pathophysiological mechanisms underlying these changes are not fully understood. It is likely that this hyper-reactivity is associated with abnormal autonomic nervous system (ANS) control. In particular, the parasympathetic (vagal) component of the ANS appears to be implicated in the pathogenesis of asthma. In addition, several studies have suggested the existence of differential alteration in ANS function following exercise in asthmatics compared with non-asthmatic individuals.Several early studies suggested that the altered autonomic control of airway calibre in asthma might be reflected by a parallel change in heart rate. Cardiac vagal reactivity does indeed appear to be increased in asthma, as demonstrated by the cardiac response to various autonomic functions tests. However, other studies have reported a lack of association between bronchial and cardiac vagal tone, and this is in accord with the concept of system-independent ANS control.This review provides a discussion of cardiovascular–autonomic changes associated with either the pathophysiology of asthma per se or with asthma pharmacotherapy treatment. Previous investigations are summarised suggesting an apparent association between altered autonomic–cardiovascular control and bronchial asthma. The full extent of autonomic dysfunction, and its clinical implications, has yet to be fully determined and should be the subject of future investigation