Postdoctoral Research Associate University of Georgia ATHENS, Georgia
Body of Abstract: Plant-parasitic cyst nematodes establish a permanent feeding site known as a syncytium within host roots to obtain nutrients. During infection, an infective juvenile will select a single cell near the vasculature and use stylet-secreted effectors to divert the cell away from its intrinsic developmental trajectory. Neighboring cells will then be gradually incorporated into the developing syncytium by cell wall dissolution and protoplasmic fusion. Cyst nematode secreted CLE-like effectors are among the most well characterized effectors that mimic plant endogenous CLE peptide hormones to promote syncytium formation. Here, using RNA-sequencing, we identified ATHB8, a member of the HD-ZIP III transcription factor family, as a potential downstream component of the CLE signaling pathway in syncytium formation. HD-ZIP III TFs function downstream of auxin signaling to promote cellular quiescence and define stem cell organizer cells in vascular patterning. Interestingly, we found that both HD-ZIP III expression and auxin response, indicated by proATHB8::4xYFP and DR5::4xYFP respectively, are highly induced in cells neighboring the syncytial cell, but not in the syncytium itself, as early as two days post-inoculation. Conversely, MIR165a, which expresses in endodermal cells and moves into vasculature to suppress HD-ZIP III TFs, is down-regulated near the infection site. Knocking down HD-ZIP III TFs by inducible over-expression of MIR165a in Arabidopsis dramatically reduced infection rate of the sugar beet cyst nematode (Heterodera schachtii). These results suggest that HD-ZIP III TFs may function as a connecting point for CLE and auxin signaling pathways in promoting syncytium formation, possibly by inducing neighboring cells into a quiescent status and priming these cells for subsequent syncytium incorporation.