3 research outputs found
Modelling broccoli development, yield and quality
Broccoli is a vegetable crop of increasing importance in Australia, particularly in south-east Queensland and farmers need to maintain a regular supply of good quality broccoli to meet the expanding market. A predictive model of ontogeny, incorporating climatic data including frost risk, would enable farmers to predict harvest maturity date and select appropriate cultivar - sowing date combinations. To develop procedures for predicting ontogeny, yield and quality, field studies using three cultivars, 'Fiesta', 'Greenbelt' and 'Marathon', were sown on eight dates from 11 March to 22 May 1997, and grown under natural and extended (16 h) photoperiods at the University of Queensland, Gatton Campus. Cultivar, rather than the environment, mainly determined head quality attributes of head shape and branching angle. Yield and quality were not influenced by photoperiod. A better understanding of genotype and environmental interactions will help farmers optimise yield and quality, by matching cultivars with time of sowing. The estimated base and optimum temperature for broccoli development were 0 degrees C and 20 degrees C, respectively, and were consistent across cultivars, but thermal time requirements for phenological intervals were cultivar specific. Differences in thermal time requirement from floral initiation to harvest maturity between cultivars were small and of little importance, but differences in thermal time requirement from emergence to floral initiation were large. Sensitivity to photoperiod and solar radiation was low in the three cultivars used. This research has produced models to assist broccoli farmers in crop scheduling and cultivar selection in south-east Queensland
Early loss of Crebbp confers malignant stem cell properties on lymphoid progenitors.
Loss-of-function mutations of cyclic-AMP response element binding protein, binding protein (CREBBP) are prevalent in lymphoid malignancies. However, the tumour suppressor functions of CREBBP remain unclear. We demonstrate that loss of Crebbp in murine haematopoietic stem and progenitor cells (HSPCs) leads to increased development of B-cell lymphomas. This is preceded by accumulation of hyperproliferative lymphoid progenitors with a defective DNA damage response (DDR) due to a failure to acetylate p53. We identify a premalignant lymphoma stem cell population with decreased H3K27ac, which undergoes transcriptional and genetic evolution due to the altered DDR, resulting in lymphomagenesis. Importantly, when Crebbp is lost later in lymphopoiesis, cellular abnormalities are lost and tumour generation is attenuated. We also document that CREBBP mutations may occur in HSPCs from patients with CREBBP-mutated lymphoma. These data suggest that earlier loss of Crebbp is advantageous for lymphoid transformation and inform the cellular origins and subsequent evolution of lymphoid malignancies