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Control of tolerance to complete and partial submergence are regulated by similar type ERF (ethylene response factor) transcription factors by opposite mechanisms.
Regulatory T cells (Tregs) are essential in the control of tolerance.
As demonstrated in TGF-β1 knockout mouse, a loss of control in apoptosis affects the development and control of tolerance.
Dendritic cells play a central role in coordinating both adaptive antimicrobial immunity and control of tolerance [ 60].
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Mapping of quantitative trait loci (QTLs) can enable dissection of the genetic control of each tolerance mechanism, opening up the possibility of future efforts to develop varieties with improved salinity tolerance by precisely transferring QTLs into popular varieties and pyramiding multiple relevant QTLs for a particular stress-prone environment.
Until the mid-1990s, the genetic control of submergence tolerance remained ambiguous.
Zhang and Hook (1992) argue that the main problem is the control of sequential tolerance, which is appropriate for those components moving in a series of consequential processes and using real-time criteria for consecutive manufacturing.
Although, the ontogenic control of postnatal tolerance is incompletely understood, the developmental changes reported in this study that coordinates the downregulation of cell surface expression of TLRs and their signaling molecules and upregulation of negative regulators is likely to be important in postnatal adaptation to initial intestinal colonization.
Genetic control of submergence tolerance was unknown until mid-1990s.
Functional analysis of these genes may provide novel insights into the genetic control of drought tolerance.
Still relatively limited information is available about the genetics and molecular control of drought tolerance.
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