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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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( 10.3390/cells8020158) [DOI] [PMC free article] [PubMed] [Google Scholar] Billeter AT, Scheurlen KM, Israel B, Straub BK, Schirmacher P, Kopf S, Nawroth PP & Muller-Stich BP 2022
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