In some instances this enhancement varies depending on the target microorganism but in other cases

This enhancement is consistent across a wide range of targets. The fact that this enhancement is apparent against Gram positive and Gram negative targets is particularly novel. Further efforts will focus on determining the mechanistic basis for these enhancements and an Mepiroxol assessment of how well these peptides perform in food and in vivo. The mechanism by which the developing crop influences return bloom and yield the following year is not fully understood. Two hypotheses have been suggested. The “nutritional” hypothesis holds that return bloom and yield are proportional to tree carbohydrate status. Lack of carbohydrate in the ON year Catharanthine sulfate directly or indirectly reduces flowering the following year. Support for this hypothesis has been provided by showing positive correlations between carbohydrate levels and AB status, whereas others have shown no consistent relationship between tree carbohydrate status and floral intensity at return bloom. The “hormonal” hypothesis proposes that developing fruit produce an inhibitor that directly or indirectly reduces flowering in the spring following the ON crop. Although a number of studies have shown correlations between abscisic acid or indole-3-acetic acid and AB status, no direct evidence has been provided for their involvement in the return bloom. Gibberellin is well-known inhibitor of flowering in citrus; thus, fruitproduced GA has been presumed to be involved in AB. Despite these findings, the roles of carbohydrates and hormones in AB remain unclear and more research is needed to identify factors affecting floral intensity following ON and OFF years. Genetic analysis of AB in apple identified a few QTLs associated with AB, and suggested that hormone-related genes are likely to play a role in the phenomenon. The floral induction period in citrus starts in mid-November and lasts until approximately the end of December to mid-January. Following induction, the bud enters a short resting period, after which the shoot apical meristem differentiates into a floral bud. In parallel to the floral shoot flush, there is a flush of vegetative shoot growth, which continues through June. A second flush of vegetative shoot growth starts in July, and third flush starts in October. Usually, next year flowering occurs mostly on the spring vegetative flush. Flowering in citrus is induced by low temperature, while day length has a relatively minor effect. There is extensive cross-talk between autonomous and vernalization flowering pathways and ample evidence that genes associated with flowering regulation are highly conserved across species. Fruit presence inhibits return flowering. However, it is not clear at which stage the fruit exerts its inhibitory effect: at flowering induction, transition of the shoot apical meristem to floral meristem, or subsequent stages of floral development and bud break. Moreover, the nature of the signal and the organ or tissue from which it originates, be it the fruit itself or the leaf which senses fruit presence, are not known. Regardless of the source tissue for the AB signal, it must be received, directly or indirectly, at the bud, and more specifically, at the apical meristem which has to “decide” whether to develop into an inflorescence or remain a vegetative meristem. Therefore, following perception of the signal, the bud must undergo a series of events which depend on fruit load. In the current work, we analyzed changes in global gene expression during bud development in ON and OFF trees, to identify metabolic and controlling pathways that play a role in bud fate. To determine the earliest time point for the transcriptome analysis, we first analyzed changes in bud morphology during its development, and changes in the expression of key flowering control genes.

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