Summary: ALTERED RESPONSE TO GRAVITY1 (ARG1) and its paralog ARG1‐LIKE2 (ARL2) are J‐domain proteins that are required for normal root and hypocotyl gravitropism. In this paper, we show that both ARL2 and ARG1 function in a gravity signal transduction pathway with PIN3, an auxin efflux facilitator that is expressed in the statocytes. In gravi‐stimulated roots, PIN3 relocalizes to the lower side of statocytes, a process that is thought to, in part, drive the asymmetrical redistribution of auxin toward the lower flank of the root. We show that ARL2 and ARG1 are required for PIN3 relocalization and asymmetrical distribution of auxin upon gravi‐stimulation. ARL2 is expressed specifically in the root statocytes, where it localizes to the plasma membrane. Upon ectopic expression, ARL2 is also found at the cell plate of dividing cells during cytokinesis, an area of intense membrane dynamics. Mutations in ARL2 and ARG1 also result in auxin‐related expansion of the root cap columella, consistent with a role for ARL2 and ARG1 in regulating auxin flux through the root tip. Together these data suggest that ARL2 and ARG1 functionally link gravity sensation in the statocytes to auxin redistribution through the root cap.

ARG1 (ALTERED RESPONSE TO GRAVITY) is required for normal root and hypocotyl gravitropism. Here, we show that targeting ARG1 to the gravity-perceiving cells of roots or hypocotyls is sufficient to rescue the gravitropic defects in the corresponding organs of arg1-2 null mutants. The cytosolic alkalinization of root cap columella cells that normally occurs very rapidly upon gravistimulation is lacking in arg1-2 mutants. Additionally, vertically grown arg1-2 roots appear to accumulate a greater amount of auxin in an expanded domain of the root cap compared with the wild type, and no detectable lateral auxin gradient develops across mutant root caps in response to gravistimulation. We also demonstrate that ARG1 is a peripheral membrane protein that may share some subcellular compartments in the vesicular trafficking pathway with PIN auxin efflux carriers. These data support our hypothesis that ARG1 is involved early in gravitropic signal transduction within the gravity-perceiving cells, where it influences pH changes and auxin distribution. We propose that ARG1 affects the localization and/or activity of PIN or other proteins involved in lateral auxin transport.

Cadaverine derives from lysine in a pathway that is distinct from that of the other well-characterized ornithine- or arginine-derived polyamines. Despite a multitude of studies in bacterial systems, cadaverine has garnered little attention in plant research. Nonetheless, many plants have been found to synthesize it. For instance, the Leguminosae have been shown to produce cadaverine and use it as a precursor in the biosynthesis of quinolizidine alkaloids, secondary metabolites that are involved in insect defense and also display therapeutic pharmacological properties. Cadaverine is also present in the environment; it can be produced by rhizosphere and phyllosphere microbes. Markedly, exogenous cadaverine application causes alterations in root-system architecture. Previous research suggests cadaverine has a role in stress response, with groups reporting an increase in content upon exposure to heat, drought, salt, and oxidative stress. However, data regarding the role of cadaverine in stress response remains conflicted, as some plant systems show enhanced tolerance to stresses in its presence, while others show increased sensitivity to the same stresses. In this review, we summarize recent findings on the role of cadaverine in plant growth, development, and stress response. We also address the possible roles rhizosphere and phyllosphere microbes may play in the delivery of exogenous cadaverine near plant organs, and discuss our current understanding of the molecular pathways that contribute to cadaverine homeostasis and response in plants.

Endoreduplication, a modified cell cycle that allows cells to increase ploidy without subsequent cell division, is a key component of plant growth and development. In this work, we show that some, but not all, of the endoreduplication of Arabidopsis (Arabidopsis thaliana) is mediated by the expression of a WD40 gene, FIZZY-RELATED2 (FZR2). Loss-of-function alleles show reduced endoreduplication and reduced expansion in trichomes and other leaf cells. Misexpression of FZR2 is sufficient to drive ectopic or extra endoreduplication in leaves, roots, and flowers, leading to alteration of cell sizes and, sometimes, organ size and shape. Our data, which suggest that reduced cell size can be compensated by increased cell proliferation to allow normal leaf morphology, are discussed with respect to the so-called compensation mechanism of plant development.