Summary• Allopolyploidy is a major driving force in plant evolution and can induce rapid structural changes in the hybrid genome. As major components of plant genomes, transposable elements are involved in these changes. In a previous work, we observed turnover of retrotransposon insertions in natural allotretraploid tobacco (Nicotiana tabacum). Here, we studied the early stages of allopolyploid formation by monitoring changes at retrotransposon insertion sites in the Th37 synthetic tobacco.• We used sequence-specific amplification polymorphism (SSAP) to study insertion patterns of two populations of the Tnt1 retrotransposon in Th37 S4 generation plants, and characterized the nature of polymorphic insertion sites.• We observed significant amplification of young Tnt1 populations. Newly transposed copies were amplified from maternal elements and were highly similar to Tnt1A tobacco copies amplified in response to microbial factors. A high proportion of paternal SSAP bands were not transmitted to the hybrid, corresponding to various rearrangements at paternal insertion sites, including indels or the complete loss of the Tnt1 ⁄ flanking junction.• These data indicate that major changes, such as retrotransposon amplification and molecular restructuring in or around insertion sites, occur rapidly in response to allopolyploidy.

apoptosis ͉ inositol phosphate ͉ lymphocyte ͉ Rasa3 C ross-linking of the antigen receptor on T and B lymphocytes by antigen is followed by the rapid activation of phospholipase C␥, resulting in the hydrolysis of phosphatidylinositol 4,5-bisphosphate and the production of inositol 1,4,5-trisphosphate [Ins(1,4,5)P 3 ] and diacylglycerol. Ins(1,4,5)P 3 causes release of calcium from the endoplasmic reticulum and is the substrate of two main metabolic pathways. Dephosphorylation by type I Ins(1,4,5)P 3 5-phosphatase generates the inactive metabolite inositol 1,4-bisphosphate (1, 2). Phosphorylation by isoforms A, B, and C of Ins(1,4,5)P 3 3-kinase (Itpkb) or inositol polyphosphate multikinase results in the production of inositol 1,3,4,5-tetrakisphosphate [Ins(1,3,4,5)P 4 ] (3). In various cellular systems, it has been demonstrated that Ins(1,3,4,5)P 4 is a modulator of Ins(1,4,5)P 3 levels and calcium mobilization (3-5). However, Ins(1,4,5)P 3 and calcium concentrations in response to T cell antigen receptor stimulation were found normal in double-positive thymocytes from Itpkb-deficient mice, despite an important decrease in Ins(1,3,4,5)P 4 production resulting in profound defects in the final maturation of these cells (6, 7). Alternative pathways to mediate the cellular effects of Ins(1,3,4,5)P 4 include the binding to pleckstrin homology (PH) domains of specific proteins acting as Ins(1,3,4,5)P 4 receptor, and the synthesis of higher inositol phosphates (8).To assess the potential contribution of the Ins(1,4,5)P 3 -ItpkbIns(1,3,4,5)P 4 signaling pathway to B cell function and development, we have analyzed the B cell lineage of Itpkb Ϫ/Ϫ mice. Our results indicate that Itpkb and Ins(1,3,4,5)P 4 mediate a survival signal in B cells by regulating Erk signaling pathway and proapoptotic Bim gene expression.

The genomic shock hypothesis suggests that allopolyploidy is associated with genome changes driven by transposable elements, as a response to imbalances between parental insertion loads. To explore this hypothesis, we compared three allotetraploids, Nicotiana arentsii, N. rustica and N. tabacum, which arose over comparable time frames from hybridisation between increasingly divergent diploid species. We used sequence-specific amplification polymorphism (SSAP) to compare the dynamics of six transposable elements in these allopolyploids, their diploid progenitors and in corresponding synthetic hybrids. We show that element-specific dynamics in young Nicotiana allopolyploids reflect their dynamics in diploid progenitors. Transposable element mobilisation is not concomitant with immediate genome merger, but occurs within the first generations of allopolyploid formation. In natural allopolyploids, such mobilisations correlate with imbalances in the repeat profile of the parental species, which increases with their genetic divergence. Other restructuring leading to locus loss is immediate, nonrandom and targeted at specific subgenomes, independently of cross orientation. The correlation between transposable element mobilisation in allopolyploids and quantitative imbalances in parental transposable element loads supports the genome shock hypothesis proposed by McClintock.