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Sharma P, Srivastava P, Seth A, Tripathi PN, Banerjee AG, Shrivastava SK

(15) Again, significant differences, I'm sure you'll agree

We therefore hypothesized that the partnership between PIF4 and other PIFs was the reason that PIF4 variants with weakened PIF4 TAD activity (e.g., mTAD and mWFYL) or DNA-binding (mB and RRQQ) could still largely complement the pif4 null mutant (Fig

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These effects could be due to knock-on impacts of the mitigation of ROS and antioxidant activation or could represent other pathways that are distinctly modulated by HG