Splice variant of the SND1 transcription factor is a dominant negative of SND1 members and their regulation in <i>Populus trichocarpa</i>

<jats:p> Secondary Wall-Associated NAC Domain 1s (SND1s) are transcription factors (TFs) known to activate a cascade of <jats:italic>TF</jats:italic> and pathway genes affecting secondary cell wall biosynthesis (xylogenesis) in <jats:italic>Arabidopsis</jats:italic> and poplars. Elevated SND1 transcriptional activation leads to ectopic xylogenesis and stunted growth. Nothing is known about the upstream regulators of <jats:italic>SND1</jats:italic> . Here we report the discovery of a stem-differentiating xylem (SDX)-specific alternative <jats:italic>SND1</jats:italic> splice variant, <jats:italic>PtrSND1</jats:italic> - <jats:italic>A2</jats:italic> <jats:sup> <jats:italic>IR</jats:italic> </jats:sup> , that acts as a dominant negative of SND1 transcriptional network genes in <jats:italic>Populus trichocarpa</jats:italic> . <jats:italic>PtrSND1</jats:italic> - <jats:italic>A2</jats:italic> <jats:sup> <jats:italic>IR</jats:italic> </jats:sup> derives from <jats:italic>PtrSND1-A2</jats:italic> , one of the four fully spliced <jats:italic>PtrSND1</jats:italic> gene family members ( <jats:italic>PtrSND1</jats:italic> - <jats:italic>A1</jats:italic> , - <jats:italic>A2</jats:italic> , - <jats:italic>B1</jats:italic> , and - <jats:italic>B2</jats:italic> ). Each full-size PtrSND1 activates its own gene, and all four full-size members activate a common <jats:italic>MYB</jats:italic> gene ( <jats:italic>PtrMYB021</jats:italic> ). PtrSND1-A2 <jats:sup>IR</jats:sup> represses the expression of its <jats:italic>PtrSND1</jats:italic> member genes and <jats:italic>PtrMYB021</jats:italic> . Repression of the autoregulation of a TF family by its only splice variant has not been previously reported in plants. PtrSND1-A2 <jats:sup>IR</jats:sup> lacks DNA binding and transactivation abilities but retains dimerization capability. PtrSND1-A2 <jats:sup>IR</jats:sup> is localized exclusively in cytoplasmic foci. In the presence of any full-size PtrSND1 member, PtrSND1-A2 <jats:sup>IR</jats:sup> is translocated into the nucleus exclusively as a heterodimeric partner with full-size PtrSND1s. Our findings are consistent with a model in which the translocated PtrSND1-A2 <jats:sup>IR</jats:sup> lacking DNA-binding and transactivating abilities can disrupt the function of full-size PtrSND1s, making them nonproductive through heterodimerization, and thereby modulating the SND1 transcriptional network. PtrSND1-A2 <jats:sup>IR</jats:sup> may contribute to transcriptional homeostasis to avoid deleterious effects on xylogenesis and plant growth. </jats:p>