Clinical and pathological study of ischaemic neuropathy.

Abstract

<h3>Abstract</h3> Pontin and Reptin are essential eukaryotic AAA+ ATPases that work together in several multiprotein complexes, contributing to chromatin remodeling and TARGET OF RAPAMCYIN (TOR) kinase complex assembly, among other functions. Null alleles of <i>pontin</i> or <i>reptin</i> are gametophyte lethal in plants, which has hindered studies of their crucial roles in plant biology. Here, we used virus-induced gene silencing (VIGS) to interrogate the functions of <i>Pontin</i> and <i>Reptin</i> in plant growth and physiology, focusing on <i>Nicotiana benthamiana</i>, a model species for the agriculturally significant <i>Solanaceae</i> family. Silencing either <i>Pontin</i> or <i>Reptin</i> caused pleiotropic developmental and physiological reprogramming, including aberrant leaf shape, reduced apical growth, delayed flowering, increased branching, chlorosis, and decreased spread of the RNA viruses <i>Tobacco mosaic virus</i> (TMV) and <i>Potato virus X</i> (PVX). To dissect these pleiotropic phenotypes, we took a comparative approach and silenced expression of key genes that encode subunits of each of the major Pontin/Reptin-associated chromatin remodeling or TOR complexes (<i>INO80</i>, <i>SWR-C/PIE1</i>, <i>TIP60</i>, <i>TOR</i>, and <i>TELO2</i>). We found that many of the <i>pontin/reptin</i> phenotypes could be attributed specifically to disruption of one of these complexes, with <i>tip60</i> and <i>tor</i> knockdown plants each phenocopying a large subset of <i>pontin/reptin</i> phenotypes. We conclude that Pontin/Reptin complexes are crucial for proper plant development, physiology, and stress responses, highlighting the multifaceted roles these conserved enzymes have evolved in eukaryotic cells.