The recognition of a positive correlation between organism genome size with its transposable element (TE) content, represents a key discovery of the field of genome biology. Considerable evidence accumulated since then suggests the involvement of TEs in genome structure, evolution and function. The global genome reorganization brought about by transposon activity might play an adaptive/regulatory role in the host response to environmental challenges, reminiscent of McClintock's original ‘Controlling Element’ hypothesis. This regulatory aspect of TEs is also garnering support in light of the recent evidences, which project TEs as “distributed genomic control modules.” According to this view, TEs are capable of actively reprogramming host genes circuits and ultimately fine-tuning the host response to specific environmental stimuli. Moreover, the stress-induced changes in epigenetic status of TE activity may allow TEs to propagate their stress responsive elements to host genes; the resulting genome fluidity can permit phenotypic plasticity and adaptation to stress. Given their predominating presence in the plant genomes, nested organization in the genic regions and potential regulatory role in stress response, TEs hold unexplored potential for crop improvement programs. This review intends to present the current information about the roles played by TEs in plant genome organization, evolution, and function and highlight the regulatory mechanisms in plant stress responses. We will also briefly discuss the connection between TE activity, host epigenetic response and phenotypic plasticity as a critical link for traversing the translational bridge from a purely basic study of TEs, to the applied field of stress adaptation and crop improvement.

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Vertical transmission of hepatitis B virus (HBV) from the mother to the newborn often results in viral persistence. To understand mechanisms of maternofetal HBV transmission, we studied maternal immunity and peripheral blood mononuclear cell (PBMC) transcriptome in mothers and newborns. We included 50 mothers and babies who were hepatitis B surface antigen (HBsAg) positive: 22 HBV transmitting mothers (group [Gr.] I) and 28 HBV nontransmitting mothers (Gr. II) to newborns and 10 healthy mother–baby pairs (Gr. III). PBMCs were analyzed for HBV‐specific dendritic cells (DCs), T cells, T follicular helper (TFh) cells, B cells, functional immune responses, and cytokine levels as well as transcriptome signatures to identify immune gene expression correlates for protective immunity. Group II mothers had lower HBsAg levels (3.82 × 10 3 versus 1.493 × 10 4 ; P < 0.0001) with greater HBV‐specific responses of DCs, T cells, TFh cells, and B cells than Gr. I mothers. Frequencies of TFh cells were lower in Gr. I mothers, with reduced interleukin‐21 (IL‐21) levels, and these inversely correlated with HBV DNA levels. Cut‐off levels of 9.5% and 8.93% from the receiver operating curve predicted the involvement of TFh cells and B cells in HBV transmission. Transcriptome signatures revealed that maternal gene imprints were reflected in the newborns. Genes related to DCs, TFh cells, and B cells were increased in Gr. II, and Gr. II newborns showed a boost in cellular and humoral responses after vaccination. Conclusion : In mothers infected with HBV, low serum IL‐21 levels and decreased TFh‐cell and plasma B‐cell frequencies are associated with vertical transmission of HBV to newborns. These features are indicative of low protective maternal immunity.