In September, buds of ‘Washington’ navel orange trees (Citrus sinensis) grown under warm, well-irrigated conditions for five months expressed FLOWERING LOCUS T (FT), SUPPRESSOR OF OVEREXPRESSION OF CONSTANS1 (SOC1), LEAFY (LFY), APETALA1 (AP1) and APETALA2 (AP2); SEPALLATA1 (SEP1), PISTILLATA (PI) and AGAMOUS (AG) were not expressed and no inflorescences developed. Subjecting the trees to low-temperature or water-deficit treatment had no effect on FT, SOC1 and LFY expression, but increased AP1 and AP2 expression with concomitant activation of SEP1, PI and AG and significant flowering. Gibberellic acid (GA3) applied to buds of low-temperature- or water-deficit-treated trees did not affect FT, SOC1 or LFY expression, but dramatically reduced AP1 and AP2 transcription, repressing SEP1, PI and AG and flowering. Similarly, buds of field-grown low-yield, off-crop ‘Pixie’ and ‘Nules Clementine’ mandarin trees (C. reticulata) collected in October expressed FT, SOC1, LFY, AP1 and AP2, with SEP1, PI and AG expression delayed until March, one month before the intense return bloom. For high-yield, on-crop trees, which failed to flower, bud FT transcripts were not detected in October through March, LFY, AP1, AP2 and SEP1 expression were lower than off-crop trees by March, and PI and AG transcripts never exceeded the limit of detection. Removing the on crop from ‘Pixie’ mandarin trees in November increased FT expression above detectable levels, AP1 to the level of off-crop trees, and activated PI and AG, resulting in a small number of inflorescence (21% of off-crop trees). To mitigate the negative effects of the on crop on return bloom and yield, fruit would need to be removed before October. Results of this research demonstrated: (i) citrus buds initiate floral development prior to exposure to low temperature in fall-winter, consistent with transition from vegetative to floral development in summer, but leaving open the possibility all buds on adult citrus trees are induced to flower; (ii) sustained FT expression is required for increased AP1 and AP2 expression to levels sufficient for floral determinacy, activation of downstream floral organ identity genes and flowering; and (iii) GA3 and the on crop of citrus fruit inhibit flowering by preventing bud determinacy, not floral induction.

Vermicompost teas (VCT) are documented to increase plant growth and yield and reduce plant fungal and bacterial diseases and nematode infestation in the soil. However, the underlying mechanisms for these results remain obscure. Radioimmnoassay was used to identify and quantify phytohormones present in commercially prepared "growth-promoting" VCT. Isopentenyladenine (IPA) and indole-3-acetic acid (IAA) were detected in VCT, along with a low amount of abscisic acid (ABA). Comparison of effects of VCT applied at the recommended rate with IPA applied at an amount equivalent to that supplied in the VCT treatment provided evidence that IPA increased Lycopersicon esculentum vegetative biomass, whereas the VCT increased fruit number per plant and fruit size. Comparison of a commercial "nematode-suppressing" nsVCT with treatments supplying equivalent amounts of IPA and IAA present in the VCT provided evidence that the nsVCT reduced galling and increased the growth of Lycopersicon esculentum plants inoculated with 5,000 and 10,000 eggs of root knot nematode (Meloidogyne incognita). The biomass plants of plants treated with nsVCT was greater or equal to that of control plants not inoculated with nematode eggs. Fungi and bacteria in the nsVCT were identified using rRNA gene analysis. Candida sp., Torulospora Sp., Saccharomyces sp. and some parasitic forms of Cladosporium sp. were dominant. The results provide the first evidence that plant hormones are present in VCT and document the growth promoting and nematode-suppressing capacity of vermicompost teas.

In alternate bearing olive trees, high yield on-crop years alternate with low yield off-crop years. Research was undertaken in support of the California olive industry to determine how fruit number one year impacts floral intensity and yield the following year. Removing the on-crop of fruit before endocarp hardening (mid-July) restored summer vegetative shoot growth and inflorescence number the following spring. Delaying fruit removal to 75 days after endocarp hardening (September) significantly reduced spring bud break and floral intensity. Quantification of the fate of buds on nonbearing and bearing shoots of off- and on-crop control trees provided striking results. The majority of buds on nonbearing shoots of off-crop trees produced inflorescences, whereas most buds on nonbearing shoots of on-crop trees remained inactive through spring bloom. In sharp contrast, 74% of buds on bearing shoots of on-crop trees had abscised prior to spring bloom. A putative O. europaea FLOWERING LOCUS T (FT) gene, known to upregulate flowering in woody perennials, was expressed in buds on nonbearing shoots of off-crop trees from June through March, but was repressed in buds of bearing and nonbearing shoots of on-crop trees starting in September and October, respectively. Whereas the lack of OeFT expression in buds on bearing shoots of on-crop trees may be due to the abscission of 51% of the floral buds by September, this result taken together with the repression of OeFT in buds on nonbearing shoots of on-crop trees in October, for which floral bud abscission was not a factor, suggests the possibility that the on crop may inhibit determination of the floral meristem between September and October. Buds on nonbearing shoots of off-crop trees subsequently expressed two floral organ identify genes in March; these genes were not expressed in buds of nonbearing and bearing shoots of on-crop trees. This study is the first to provide evidence that several mechanisms in addition to inhibition of summer vegetative shoot growth, including inhibition of spring bud break, inhibition of floral development at the level of gene expression, and abscission of potential floral buds, contribute to the perpetuation of alternate bearing in olive.