Gene expression in two cultivars of Brassica napus (AC Excel and DH12075) has been compared at the full-size embryo, desiccation, and mature stages of seed development. Seed of these cultivars differ in their potential to exhibit secondary dormancy following environmental stress; Excel has high potential and DH12075 has low potential. A majority of genes were down-regulated during maturation in both cultivars but a significant number of differences in gene expression between the cultivars were apparent in the transition from full-size embryo to mature seed. However, most differences were apparent in the desiccation stage and some of the differences were in genes related to signaling processes and protein biosynthesis. We suggest that the propensity of Brassica seeds to manifest secondary dormancy may be determined by changes in gene expression that occur during late seed development.
In the male sterile32 (ms32) mutant in Arabidopsis thaliana, pollen development is affected during meiosis of pollen mother cells (PMCs). In normal wildtype (WT) anthers, callose is deposited around PMCs before and during meiosis, and after meiosis the tetrads have a complete callose wall. In ms32, PMCs showed initial signs of some callose deposition before meiosis, but it was degraded soon after, as was part of the cellulosic wall around the PMCs. The early dissolution of callose in ms32 was associated with the occurrence of extensive stacks of rough ER (RER) in tapetal cells. The stacks of RER were also observed in the WT tapetum, but at a later stage, i.e., after the tetrads were formed and when callose is normally broken down for release of microspores. Based on these observations it is suggested that: (1) callose degradation around developing microspores is linked to the formation of RER in tapetal cells, which presumably synthesize and/or secrete callase into the anther locule, and (2) mutation in MS32 disrupts the timing of these events.
Earlier, we reported that mutation in the Male Sterile33 (MS33) locus in Arabidopsis thaliana causes inhibition of stamen filament growth and a defect in the maturation of pollen grains [Fei and Sawhney (1999) Physiol Plant 105:165-170; Fei and Sawhney (2001) Can J Bot 79:118-129]. Here we report that the ms33 mutant has other pleiotropic effects, including aberrant growth of all floral organs and a delay in seed germination and in flowering time. These defects could be partially or completely restored by low temperature or by exogenous gibberellin A4 (GA4), which in all cases was more effective than GA3. Analysis of endogenous GAs showed that in wild type (WT) mature flowers GA4 was the major GA, and that relative to WT the ms33 flowers had low levels of the growth active GAs, GA1 and GA4, and very reduced levels of GA9, GA24 and GA15, precursors of GA4. This suggests that mutation in the MS33 gene may suppress the GA biosynthetic pathway that leads to GA4 via GA9 and the early 13-H C20 GAs. WT flowers also possessed a much higher level of indole-3-acetic acid (IAA), and a lower level of abscisic acid (ABA), relative to ms33 flowers. Low temperature induced partial restoration of male fertility in the ms33 flowers and this was associated with partial increase in GA4. In contrast, in WT flowers GA1 and GA4 were very much reduced by low temperature. Low temperature also had little effect on IAA or ABA levels of ms33 flowers, but did reduce (>2-fold) IAA levels in WT flowers. The double mutants, ms33 aba1-1 (an ABA-deficient mutant), and ms33 spy-3 (a GA signal transduction mutant) had flower phenotypes similar to ms33. Together, the data suggest that the developmental defects in the ms33 mutant are unrelated to ABA levels, but may be causally associated with reduced levels of IAA, GA1 and GA4, compared to WT flowers.
The MS33 gene in Arabidopsis is required for stamen filament growth and for pollen maturation. The objective of this study was to characterize the effects of ms33 mutation on pollen development at the ultrastructural level. There were no differences between the wild type and ms33 mutant pollen development before the first mitotic division of microspores. At the bicellular pollen stage, the first signs of abnormalities were observed in the ms33 tapetum, which started to degenerate early and released osmiophilic material in the anther locule. In ms33 pollen, the endintine was thicker, and exintine thinner, than in the wild type, and the mutant pollen had large vacuoles. Later in development, the mutant pollen underwent second mitosis and produced two normal-looking sperm cells; however, the intine was precociously formed, and there were abnormalities in tryphine deposition on the pollen wall, in the size of vacuoles, and in the formation of lipid bodies in the vegetative cell cytoplasm. Based on these observations it is suggested that mutation in the MS33 gene interferes with intine formation and tryphine deposition, both of which negatively affect pollen desiccation resulting in large, highly vacuolate pollen that are nonviable.Key words: Arabidopsis, male sterility, mutant, pollen, tapetum, ultrastructure.
The rapid growth of stamen filaments just before flower anthesis in Arabidopsis thaliana does not occur in the male sterile33 (ms33, formerly known as msZ) mutant. ms33 filaments were approximately 40% shorter than the wild type (WT), and there was corresponding reduction in the epidermal cell length of filaments. This suggests that MS33 controls the final cell‐elongation phase of filament growth. Both low temperatures and gibberellic acid (GA3) restored filament and cell growth in intact ms33 flowers, but these treatments only had a small promotive effect on WT filaments. Decapitation experiments involving the removal of the anther had the opposite effect on WT and ms33 filaments; growth was inhibited in WT, but was increased in ms33 filaments. In young stamen primordia cultured in vitro, filament growth was less in WT, but more in ms33, than in respective in vivo produced filaments. Plant growth substances (PGSs), GA3 and indole‐3‐acetic acid (IAA) were promotive, zeatin had no effect, and abscisic acid (ABA) and ethrel inhibited filament growth in both intact and decapitated WT and ms33 filaments. Together these observations suggest that MS33 is activated immediately before anthesis and that the MS33 product either regulates temporal biosynthesis of gibberellins (GAs) and/or IAA or makes the filament tissue sensitive to these PGSs, which in turn trigger cell elongation and filament growth. The data also suggest that ms33 mutant anthers contain a relatively high ratio of growth inhibitors to promoters, which inhibits epidermal cell elongation and filament growth.
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