Chemical thinning of European pear cultivars (Pyrus communis L.)

Thesis (MScAgric (Horticulture))--Stellenbosch University, 2008.Chemical thinning of fruit trees has become a central management practice for ensuring high fruit quality at harvest and return bloom the following season. Three trials were conducted in the 2004/5, 2006/7 and 2007/8 seasons to investigate the efficacy and mode of action of chemical thinning agents on European pear cultivars (Pyrus communis L) in the Western Cape, South Africa. The first trial was conducted in the 2004/5 and 2006/7 seasons to evaluate the efficacy of 50, 100 and 150 mg.l-1 6-benzyladenine (BA), and 30 and 40 mg.l-1 naphthylacetamide (NAD) on ‘Early Bon Chrétien’ pear. BA was more effective than NAD in reducing crop load and improving fruit size. Crop load decreased and fruit size increased with increasing rate of BA. BA significantly improved, whilst NAD failed to improve return bloom. In the second trial, three experiments were conducted in the 2006/7 and 2007/8 seasons to evaluate the efficacy of 100 to 200 mg.l-1 BA on ‘Forelle’ pear. The first experiment was conducted in the 2006/7 season where BA rates of 100, 125 and 150 mg.l-1 generally failed to reduce crop load or to improve fruit size and fruit size distribution and return bloom. The second experiment was conducted in the 2007/8 season where two BA rates, 150 and 200 mg.l-1 and a split-application of 3 x 50 mg.l-1 improved fruit size. The 200 mg.l-1 rate was the most effective treatment. BA did not improve fruit size distribution and return bloom. The third experiment was conducted in the 2007/8 season where the effect of rate and timing of BA applications was evaluated. Two rates, 150 and 200 mg.l-1 were applied 8, 11 and 17 days after full bloom (d.a.f.b.). There was no significant interaction between BA rate and application time. The 200 mg.l-1 rate and the 11 d.a.f.b. (i.e. 8 to 10 mm average fruit size) applications were more effective in reducing crop load, and improving fruit size. BA at 150 and 200 mg.l-1 and at all application times significantly improved return bloom relative to the control. From these trials we concluded that BA is a reliable thinner for ‘Early Bon Chrétien’ at rates of 100 or 150 mg.l-1. On ‘Forelle’, BA is not a reliable thinner and we recommended further trials with BA in combination with other thinning agents. In the third trial, three experiments were conducted in the 2007/8 season to investigate the mode of action and effect of BA application time on European pear cultivars. The effect of site of application, bourse shoot growth and fruit size at time of application on the efficacy of BA was evaluated. Results from the experiments on the effect of site of application and bourse shoot growth were inconclusive. In terms of fruit abscission, there was a significant interaction between BA application time and fruitlet size. Early BA applications (8 d.a.f.b.) were significantly more effective in promoting fruit abscission, than later (11 and 17 d.a.f.b.) applications. Smaller fruit (6 to 8 mm) were found to be more susceptible to BA-induced fruit abscission than bigger fruit (8 to 12 mm)

Initial bud outgrowth occurs independent of auxin flow out of buds

Apical dominance is the process whereby the shoot tip inhibits the growth of axillary buds along the stem. It has been proposed that the shoot tip, which is the predominant source of the plant hormone auxin, prevents bud outgrowth by suppressing auxin canalization and export from axillary buds into the main stem. In this theory, auxin flow out of axillary buds is a prerequisite for bud outgrowth and buds are triggered to grow by an enhanced proportional flow of auxin from the buds. A major challenge of directly testing this model is in being able to create a bud- or stem-specific change in auxin transport. Here we evaluate the relationship between specific changes in auxin efflux from axillary buds and bud outgrowth after shoot tip removal (decapitation) in pea (Pisum sativum L.). The auxin transport inhibitor 1-N-Naphthylphthalamic acid (NPA) and to a lesser extent, the auxin perception inhibitor p-chlorophenoxyisobutyric acid (PCIB), effectively blocked auxin efflux from axillary buds of intact and decapitated plants without affecting auxin flow in the main stem. Gene expression analyses indicate that NPA and PCIB regulate auxin-inducible, and biosynthesis and transport genes in axillary buds within 3 hours after application. These inhibitors had no effect on initial bud outgrowth after decapitation or cytokinin (benzyladenine; BA) treatment. Inhibitory effects of PCIB and NPA on axillary bud outgrowth only became apparent from 48 hours after treatment. These findings demonstrate that the initiation of decapitation- and cytokinin-induced axillary bud outgrowth is independent of auxin canalization and export from the bud

An update on the signals controlling shoot branching

Many new questions on the regulation of shoot branching have been raised in recent years, prompting a review and reassessment of the role of each signal involved. Sugars and their signaling networks have been attributed a major role in the early events of axillary bud outgrowth, whereas cytokinin appears to play a critical role in the modulation of this process in response to the environment. Perception of the recently discovered hormone strigolactone is now quite well understood, while the downstream targets remain largely unknown. Recent literature has highlighted that auxin export from a bud is important for its subsequent growth.</p

De novo transcriptome assembly and annotation for gene discovery in avocado, macadamia and mango

Avocado (Persea americana Mill.), macadamia (Macadamia integrifolia L.) and mango (Mangifera indica L.) are important subtropical tree species grown for their edible fruits and nuts. Despite their commercial and nutritional importance, the genomic information for these species is largely lacking. Here we report the generation of avocado, macadamia and mango transcriptome assemblies from pooled leaf, stem, bud, root, floral and fruit/nut tissue. Using normalized cDNA libraries, we generated comprehensive RNA-Seq datasets from which we assembled 63420, 78871 and 82198 unigenes of avocado, macadamia and mango, respectively using a combination of de novo transcriptome assembly and redundancy reduction. These unigenes were functionally annotated using Basic Local Alignment Search Tool (BLAST) to query the Universal Protein Resource Knowledgebase (UniProtKB). A workflow encompassing RNA extraction, library preparation, transcriptome assembly, redundancy reduction, assembly validation and annotation is provided. This study provides avocado, macadamia and mango transcriptome and annotation data, which is valuable for gene discovery and gene expression profiling experiments as well as ongoing and future genome annotation and marker development applications

Auxin-independent effects of apical dominance induce changes in phytohormones correlated with bud outgrowth

The inhibition of shoot branching by the growing shoot tip of plants, termed apical dominance, was originally thought to be mediated by auxin. Recently, the importance of the shoot tip sink strength during apical dominance has re-emerged with recent studies highlighting roles for sugars in promoting branching. This raises many unanswered questions on the relative roles of auxin and sugars in apical dominance. Here we show that auxin depletion after decapitation is not always the initial trigger of rapid cytokinin (CK) increases in buds that are instead correlated with enhanced sugars. Auxin may also act through strigolactones (SLs) which have been shown to suppress branching after decapitation, but here we show that SLs do not have a significant effect on initial bud outgrowth after decapitation. We report here that when sucrose or CK is abundant, SLs are less inhibitory during the bud release stage compared to during later stages and that SL treatment rapidly inhibits CK accumulation in pea (Pisum sativum) axillary buds of intact plants. After initial bud release, we find an important role of gibberellin (GA) in promoting sustained bud growth downstream of auxin. We are, therefore, able to suggest a model of apical dominance that integrates auxin, sucrose, SLs, CKs, and GAs and describes differences in signalling across stages of bud release to sustained growth

Trehalose 6-phosphate is involved in triggering axillary bud outgrowth in garden pea (Pisum sativum L.)

Trehalose 6-phosphate (Tre6P) is a signal of sucrose availability in plants, and has been implicated in the regulation of shoot branching by the abnormal branching phenotypes of Arabidopsis (Arabidopsis thaliana) and maize (Zea mays) mutants with altered Tre6P metabolism. Decapitation of garden pea (Pisum sativum) plants has been proposed to release the dormancy of axillary buds lower down the stem due to changes in sucrose supply, and we hypothesized that this response is mediated by Tre6P. Decapitation led to a rapid and sustained rise in Tre6P levels in axillary buds, coinciding with the onset of bud outgrowth. This response was suppressed by simultaneous defoliation that restricts the supply of sucrose to axillary buds in decapitated plants. Decapitation also led to a rise in amino acid levels in buds, but a fall in phosphoenolpyruvate and 2-oxoglutarate. Supplying sucrose to stem node explants in vitro triggered a concentration-dependent increase in the Tre6P content of the buds that was highly correlated with their rate of outgrowth. These data show that changes in bud Tre6P levels are correlated with initiation of bud outgrowth following decapitation, suggesting that Tre6P is involved in the release of bud dormancy by sucrose. Tre6P might also be linked to a reconfiguration of carbon and nitrogen metabolism to support the subsequent growth of the bud into a new shoot

Sucrose represses the expression of the strigolactone signalling gene D3/RMS4/MAX2 to promote tillering

Shoot branching, which is regulated by a complex signalling network, is a major component of plant architecture and therefore of crop yield. Sugars, acting in a network with hormones, have recently emerged as key players in the control of shoot branching. Previous studies in dicotyledonous plants have shown that sucrose suppresses the inhibitory effect of the plant hormone strigolactone (SL) during this process. The molecular mechanisms underlying this effect are unknown. Here we show that sucrose could antagonise the suppressive action of SL on tillering in rice. At the mechanistic level, we revealed that sucrose alleviates SL-mediated degradation of D53. Increase in sucrose availability inhibits the expression of D3 , which encodes the orthologue of the arabidopsis F-box MAX2 required for SL signalling. Over-expression of D3 prevented sucrose from inhibiting D53 degradation and enabled the SL inhibition of tillering under high sucrose. The enhanced bud elongation of the d3 mutant to sucrose treatment indicates that suppressed SL perception reduces the minimum amount of sucrose required for sustained bud outgrowth. Decapitation and sugar feeding experiments in pea indicate that RMS4 , the D3/MAX2 orthologue in pea, is also involved in the interactions between sucrose and SL. This work shows that D3/MAX2/RMS4 is a key component in the integrating both SL and sugar pathways during the regulation of shoot architecture

Sucrose promotes D53 accumulation and tillering in rice

International audienceShoot branching is regulated by multiple signals. Previous studies have indicated that sucrose may promote shoot branching through suppressing the inhibitory effect of the hormone strigolactone (SL). However, the molecular mechanisms underlying this effect are unknown. Here, we used molecular and genetic tools to identify the molecular targets underlying the antagonistic interaction between sucrose and SL. We showed that sucrose antagonizes the suppressive action of SL on tillering in rice and on the degradation of D53, a major target of SL signalling. Sucrose inhibits the gene expression of D3, the orthologue of the Arabidopsis F-box MAX2 required for SL signalling. Overexpression of D3 antagonizes sucrose inhibition of D53 degradation and enables the SL inhibition of tillering under high sucrose. Sucrose prevents SL-induced degradation of D14, the SL receptor involved in D53 degradation. In contrast to D3, D14 overexpression enhances D53 protein levels and sucrose-induced tillering, even in the presence of SL. Our results show that sucrose inhibits SL response by affecting key components of SL signalling and, together with previous studies reporting the inhibition of SL synthesis by nitrate and phosphate, demonstrate the central role played by SLs in the regulation of plant architecture by nutrients