Cytokinin Modulates Cellular Trafficking and the Cytoskeleton, Enhancing Defense Responses

The plant hormone cytokinin (CK) plays central roles in plant development and throughout plant life. The perception of CKs initiating their signaling cascade is mediated by histidine kinase receptors (AHKs). Traditionally thought to be perceived mostly at the endoplasmic reticulum (ER) due to receptor localization, CK was recently reported to be perceived at the plasma membrane (PM), with CK and its AHK receptors being trafficked between the PM and the ER. Some of the downstream mechanisms CK employs to regulate developmental processes are unknown. A seminal report in this field demonstrated that CK regulates auxin-mediated lateral root organogenesis by regulating the endocytic recycling of the auxin carrier PIN1, but since then, few works have addressed this issue. Modulation of the cellular cytoskeleton and trafficking could potentially be a mechanism executing responses downstream of CK signaling. We recently reported that CK affects the trafficking of the pattern recognition receptor LeEIX2, influencing the resultant defense output. We have also recently found that CK affects cellular trafficking and the actin cytoskeleton in fungi. In this work, we take an in-depth look at the effects of CK on cellular trafficking and on the actin cytoskeleton in plant cells. We find that CK influences the actin cytoskeleton and endomembrane compartments, both in the context of defense signaling—where CK acts to amplify the signal—as well as in steady state. We show that CK affects the distribution of FLS2, increasing its presence in the plasma membrane. Furthermore, CK enhances the cellular response to flg22, and flg22 sensing activates the CK response. Our results are in agreement with what we previously reported for fungi, suggesting a fundamental role for CK in regulating cellular integrity and trafficking as a mechanism for controlling and executing CK-mediated processes.

The evolutionary origins of auxin transport: what we know and what we need to know

Auxin, represented by indole-3-acetic acid (IAA), has for a long time been studied mainly with respect to the development of land plants, and recent evidence confirms that canonical nuclear auxin signaling is a land plant apomorphy. Increasing sequential and physiological data show that the presence of auxin transport machinery pre-dates the emergence of canonical signaling. In this review, we summarize the present state of knowledge regarding the origins of auxin transport in the green lineage (Viridiplantae), integrating both data from wet lab experiments and sequence evidence on the presence of PIN-FORMED (PIN), PIN-LIKES (PILS), and AUXIN RESISTANT 1/LIKE-AUX1 (AUX1/LAX) homologs. We discuss a high divergence of auxin carrier homologs among algal lineages and emphasize the urgent need for the establishment of good molecular biology models from within the streptophyte green algae. We further postulate and discuss two hypotheses for the ancestral role of auxin in the green lineage. First, auxin was present as a by-product of cell metabolism and the evolution of its transport was stimulated by the need for IAA sequestration and cell detoxification. Second, auxin was primarily a signaling compound, possibly of bacterial origin, and its activity in the pre-plant green algae was a consequence of long-term co-existence with bacteria in shared ecological consortia.

PILS6 is a temperature-sensitive regulator of nuclear auxin input and organ growth in Arabidopsis thaliana

Temperature modulates growth and development throughout the entire lifecycle of a plant. High temperature (HT) triggers the auxin biosynthesis-dependent growth in aerial tissues. On the other hand, the contribution of auxin to HT-induced root growth is currently under debate. Here we show that the putative intracellular auxin carrier PIN-LIKES 6 (PILS6) is a negative regulator of organ growth and that its abundance is highly sensitive to HT. PILS6 localizes to the endoplasmic reticulum and limits the nuclear availability of auxin, consequently reducing the auxin signaling output. HT represses the PILS6 protein abundance, which impacts on PILS6-dependent auxin signaling in roots and root expansion. Accordingly, we hypothesize that PILS6 is part of an alternative mechanism linking HT to auxin responses in roots.

PIN7 auxin carrier is a terminator of radial root expansion in Arabidopsis thaliana

Directional growth of lateral roots is critical for radial expansion and soil coverage. Despite its importance, almost nothing is known about its molecular determinants. Initially, young lateral roots (LRs) grow away from the parental root maintaining the angle acquired shortly after emergence. A second downwards bending response to gravity terminates the so-called plateau phase and thereby limits the radial root expansion. Here we show that the exit from the plateau phase correlates with an increase in auxin signalling at the tip of LRs. Moreover, the increase in auxin levels induces the termination of the plateau phase, which requires PIN auxin efflux carriers. Our data suggests that the developmental increase of auxin triggers the preferential de-repression of PIN7 in gravity-sensing columella cells. The subsequent polarization of PIN7 heralds the bending towards gravity and, hence, the exit from the plateau phase. This developmental framework reveals the distinct roles of PIN auxin efflux carriers in controlling the radial growth of root systems.

PILS6 is a temperature-sensitive regulator of nuclear auxin input and organ growth in Arabidopsis thaliana

Global warming is threatening plant productivity, because plant growth is highly sensitive to elevated temperatures. High temperature (HT) triggers the auxin biosynthesis-dependent growth in aerial tissues. On the other hand, the contribution of auxin to HT-induced root growth is currently under debate. Here we show that the putative intracellular auxin carrier PIN-LIKES 6 (PILS6) is a negative regulator of organ growth and that its abundance is highly sensitive to HT. PILS6 localises to the endoplasmic reticulum (ER) and limits the nuclear availability of auxin, consequently reducing the auxin signalling output. HT represses the transcription and protein abundance of PILS6 specifically in the root tip, which impacts on PILS6-dependent root organ growth rates. Accordingly, we hypothesize that PILS6 is part of a novel mechanism, linking HT to auxin responses in roots.