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Rujin Chen

Publications and source records attributed to Rujin Chen.

6 recordsLinked to original sources

Loss of At4 function impacts phosphate distribution between the roots and the shoots during phosphate starvation.

Plants display a range of adaptive responses to phosphate (Pi) starvation including an increase in the proportion of Pi allocated to the roots, which enhances lateral root development and consequently Pi acquisition. The mechanisms by which plants sense Pi and signal Pi reallocation are largely unknown. Previously, we cloned At4, a gene predicted to contain multiple short open-reading frames (ORFs), whose expression is strongly induced by Pi starvation. At4 is a member of a small gene family whose members, AtIPS1 and two additional genes reported here, At4.1 and At4.2, share little conservation among the predicted ORFs but high conservation of a 22-nt sequence located in the 3' half of the transcript. Here, we show that under Pi-starvation conditions, At4 is expressed in the vascular tissue and transcript levels are regulated by both cytokinin and ABA. at4, an At4 loss-of-function mutant fails to redistribute Pi to the roots correctly in response to Pi deprivation and At4 shoots continue to accumulate a greater proportion of Pi relative to wild type. Consistent with this, the primary root growth rate in at4 is faster than wild type in low-Pi conditions. The conserved sequence found in all members of the At4 gene family hybridizes to a small RNA present in Pi-starved roots. These data support a role for At4 in the internal allocation of Pi and suggest that the At4 gene is not only subject to Pi-starvation-inducible expression, but that transcript levels may be adjusted at a post-transcriptional level by the activity of an miRNA.

Abscisic Acid↗

Complex regulation of Arabidopsis AGR1/PIN2-mediated root gravitropic response and basipetal auxin transport by cantharidin-sensitive protein phosphatases.

Polar auxin transport, mediated by two distinct plasma membrane-localized auxin influx and efflux carrier proteins/complexes, plays an important role in many plant growth and developmental processes including tropic responses to gravity and light, development of lateral roots and patterning in embryogenesis. We have previously shown that the Arabidopsis AGRAVITROPIC 1/PIN2 gene encodes an auxin efflux component regulating root gravitropism and basipetal auxin transport. However, the regulatory mechanism underlying the function of AGR1/PIN2 is largely unknown. Recently, protein phosphorylation and dephosphorylation mediated by protein kinases and phosphatases, respectively, have been implicated in regulating polar auxin transport and root gravitropism. Here, we examined the effects of chemical inhibitors of protein phosphatases on root gravitropism and basipetal auxin transport, as well as the expression pattern of AGR1/PIN2 gene and the localization of AGR1/PIN2 protein. We also examined the effects of inhibitors of vesicle trafficking and protein kinases. Our data suggest that protein phosphatases, sensitive to cantharidin and okadaic acid, are likely involved in regulating AGR1/PIN2-mediated root basipetal auxin transport and gravitropism, as well as auxin response in the root central elongation zone (CEZ). BFA-sensitive vesicle trafficking may be required for the cycling of AGR1/PIN2 between plasma membrane and the BFA compartment, but not for the AGR1/PIN2-mediated root basipetal auxin transport and auxin response in CEZ cells.

Arabidopsis↗

The promotion of gravitropism in Arabidopsis roots upon actin disruption is coupled with the extended alkalinization of the columella cytoplasm and a persistent lateral auxin gradient.

The actin cytoskeleton has been implicated in regulating plant gravitropism. However, its precise role in this process remains uncertain. We have shown previously that disruption of the actin cytoskeleton with Latrunculin B (Lat B) strongly promoted gravitropism in maize roots. These effects were most evident on a clinostat as curvature that would exceed 90 degrees despite short periods of horizontal stimulation. To probe further the cellular mechanisms underlying these enhanced gravity responses, we extended our studies to roots of Arabidopsis. Similar to our observations in other plant species, Lat B enhanced the response of Arabidopsis roots to gravity. Lat B (100 nm) and a stimulation time of 5-10 min were sufficient to induce enhanced bending responses during clinorotation. Lat B (100 nm) disrupted the fine actin filament network in different regions of the root and altered the dynamics of amyloplasts in the columella but did not inhibit the gravity-induced alkalinization of the columella cytoplasm. However, the duration of the alkalinization response during continuous gravistimulation was extended in Lat B-treated roots. Indirect visualization of auxin redistribution using the DR5:beta-glucuronidase (DR5:GUS) auxin-responsive reporter showed that the enhanced curvature of Lat B-treated roots during clinorotation was accompanied by a persistent lateral auxin gradient. Blocking the gravity-induced alkalinization of the columella cytoplasm with caged protons reduced Lat B-induced curvature and the development of the lateral auxin gradient. Our data indicate that the actin cytoskeleton is unnecessary for the initial perception of gravity but likely acts to downregulate gravitropism by continuously resetting the gravitropic-signaling system.

Actins↗

ALTERED RESPONSE TO GRAVITY is a peripheral membrane protein that modulates gravity-induced cytoplasmic alkalinization and lateral auxin transport in plant statocytes.

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.

Arabidopsis↗

Complex physiological and molecular processes underlying root gravitropism.

Gravitropism allows plant organs to guide their growth in relation to the gravity vector. For most roots, this response to gravity allows downward growth into soil where water and nutrients are available for plant growth and development. The primary site for gravity sensing in roots includes the root cap and appears to involve the sedimentation of amyloplasts within the columella cells. This process triggers a signal transduction pathway that promotes both an acidification of the wall around the columella cells, an alkalinization of the columella cytoplasm, and the development of a lateral polarity across the root cap that allows for the establishment of a lateral auxin gradient. This gradient is then transmitted to the elongation zones where it triggers a differential cellular elongation on opposite flanks of the central elongation zone, responsible for part of the gravitropic curvature. Recent findings also suggest the involvement of a secondary site/mechanism of gravity sensing for gravitropism in roots, and the possibility that the early phases of graviresponse, which involve differential elongation on opposite flanks of the distal elongation zone, might be independent of this auxin gradient. This review discusses our current understanding of the molecular and physiological mechanisms underlying these various phases of the gravitropic response in roots.

Gravitropism↗