1.
GmPTF1 modifies root architecture responses to phosphate starvation primarily through regulating GmEXPB2 expression in soybean.
Yang, Z, Gao, Z, Zhou, H, He, Y, Liu, Y, Lai, Y, Zheng, J, Li, X, Liao, H
The Plant journal : for cell and molecular biology. 2021;(2):525-543
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Abstract
Though root architecture modifications may be critically important for improving phosphorus (P) efficiency in crops, the regulatory mechanisms triggering these changes remain unclear. In this study, we demonstrate that genotypic variation in GmEXPB2 expression is strongly correlated with root elongation and P acquisition efficiency, and enhancing its transcription significantly improves soybean yield in the field. Promoter deletion analysis was performed using 5' truncation fragments (P1-P6) of GmEXPB2 fused with the GUS gene in soybean transgenic hairy roots, which revealed that the P1 segment containing three E-box elements significantly enhances induction of gene expression in response to phosphate (Pi) starvation. Further experimentation demonstrated that GmPTF1, a basic-helix-loop-helix transcription factor, is the regulatory factor responsible for the induction of GmEXPB2 expression in response to Pi starvation. In short, Pi starvation induced expression of GmPTF1, with the GmPTF1 product directly binding to the E-box motif in the P1 region of the GmEXPB2 promoter. Plus, both GmPTF1 and GmEXPB2 highly expressed in lateral roots, and were significantly enhanced by P deficiency. Further work with soybean stable transgenic plants through RNA sequencing analysis showed that altering GmPTF1 expression significantly impacted the transcription of a series of cell wall genes, including GmEXPB2, and thereby affected root growth, biomass and P uptake. Taken together, this work identifies a novel regulatory factor, GmPTF1, involved in changing soybean root architecture partially through regulation of the expression of GmEXPB2 by binding the E-box motif in its promoter region.
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Divergence involving global regulatory gene mutations in an Escherichia coli population evolving under phosphate limitation.
Wang, L, Spira, B, Zhou, Z, Feng, L, Maharjan, RP, Li, X, Li, F, McKenzie, C, Reeves, PR, Ferenci, T
Genome biology and evolution. 2010;:478-87
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Abstract
Many of the important changes in evolution are regulatory in nature. Sequenced bacterial genomes point to flexibility in regulatory circuits but we do not know how regulation is remodeled in evolving bacteria. Here, we study the regulatory changes that emerge in populations evolving under controlled conditions during experimental evolution of Escherichia coli in a phosphate-limited chemostat culture. Genomes were sequenced from five clones with different combinations of phenotypic properties that coexisted in a population after 37 days. Each of the distinct isolates contained a different mutation in 1 of 3 highly pleiotropic regulatory genes (hfq, spoT, or rpoS). The mutations resulted in dissimilar proteomic changes, consistent with the documented effects of hfq, spoT, and rpoS mutations. The different mutations do share a common benefit, however, in that the mutations each redirect cellular resources away from stress responses that are redundant in a constant selection environment. The hfq mutation lowers several individual stress responses as well the small RNA-dependent activation of rpoS translation and hence general stress resistance. The spoT mutation reduces ppGpp levels, decreasing the stringent response as well as rpoS expression. The mutations in and upstream of rpoS resulted in partial or complete loss of general stress resistance. Our observations suggest that the degeneracy at the core of bacterial stress regulation provides alternative solutions to a common evolutionary challenge. These results can explain phenotypic divergence in a constant environment and also how evolutionary jumps and adaptive radiations involve altered gene regulation.