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- Augstein, Frauke
(författare)
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Mechanisms of plant root xylem developmental plasticity in response to water deficiency and salt
- 2022
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Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- Plants may be exposed to a variety of different environmental conditions including water deficiency and salt, both affecting the uptake of water into the plant. Water is taken up from the soil by the roots and distributed throughout the plant via the water conducting tissue, the xylem. Plants are remarkably plastic and have evolved different mechanisms to sense the environment and adjust their development accordingly. However, how xylem development may respond to water availability is not clear. In this thesis, I show how water deficiency and salt affect xylem development and how the observed phenotypic alterations are regulated on a molecular level. We found that upon water deficiency additional protoxylem strands were formed along with an early differentiation of the inner metaxylem. These phenotypes were regulated both by non-cell autonomous and cell autonomous signaling via the hormone abscisic acid (ABA). The expression of microRNA165 was induced by ABA signaling in the endodermis leading to downregulation of homeo domain leucine zipper class III (HD-ZIP III) transcription factors in the stele. This caused a shift in xylem identity from meta- to protoxylem and the formation of additional protoxylem strands. At the same time, cell autonomous ABA signaling upregulated several VASCULAR RELATED NAC DOMAIN (VND) transcription factors including VND7, which promoted the shift in xylem identity as well as VND2 and VND3, which promoted early differentiation of the inner metaxylem. In contrast, during an initial phase of salt stress, we observed the formation of protoxylem gaps specifically in response to ionic stress and distinct from ABA-signaling. We identified that protoxylem gaps were caused by lowered levels and signaling of the growth regulator gibberellin (GA). Downstream of GA-signaling, protoxylem gap formation upon salt was controlled by genes involved in secondary cell wall formation including the xylem master regulator VND6 and factors involved in cell wall modification. Salt tolerance assays suggested that protoxylem gaps may contribute to salt tolerance and the phenotypes that we observed upon water deficiency have been suggested to confer drought tolerance. We observed similar effects on xylem developmental plasticity in response to water deficiency and salt in various different dicot species indicating an evolutionary conservation. Thus, xylem development is of high relevance for breeding programs to generate plant varieties better adapted to a changing climate.
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| 2. |
- Lakehal, Abdellah, 1984-
(författare)
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A molecular network mediating adventitious root initiation in Arabidopsis thaliana
- 2019
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Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- To adapt to the ever-changing rhizosphere conditions, land plants evolved a sophisticated root system. The genetic determinants of the root system establishment have been the targets of natural selection, resulting in a very complex but robust molecular networks and circuits. These networks provide the plant with precise cell-fate and developmental decisions. The plant root system consists of primary root, lateral roots and often adventitious roots (ARs). ARs derive from the aboveground organs in response to either intrinsic developmental cues or in response to the environmental ones. AR formation is a pre-requisite step for vegetative propagation, which is widely used to multiply elite genotypes in forestry and agriculture. The main focus of this study is to unravel the molecular networks controlling AR initiation (ARI) using the intact-etiolated Arabidopsis hypocotyl as a model system. Previous data from our laboratory showed that ARI in Arabidopsis is controlled by a crosstalk between the positive regulator auxin (IAA) and the negative regulator jasmonate (JA). First, combining genetic, biochemical and hormonomics approaches, we identified the auxin coreceptor complexes involved in ARI. We found that IAA is perceived by two F-box proteins (TRANSPORT INHIBITOR1/AUXIN-SIGNALLING F-BOX (TIR1) and its closest homolog AFB2 as well as three Auxin/Inodole-3-acetic acid (Aux/IAA) repressors (IAA6, IAA9 and IAA17). These coreceptor proteins possibly act in combinatorial manner to fine-tune the auxin signaling machinery during ARI. In addition, in a genetic screen, we also revealed that the COP9 SIGNALOSOME SUBUNIT 4 (CSN4) protein plays a central role in ARI by modulating the function of the auxin perception machinery. Next, in silico search for genes acting downstream of JA involved in ARI, we retrieved the recently characterized DIOXYGENASE FOR AUXIN OXIDATION (DAO1) and DAO2 genes. The DAOs encode for enzymes that catalyze the conversion of free IAA into 2-oxindole-3-acetic acid (oxIAA), a rate-limiting step in auxin degradation. We found that the DAO1 gene mediates a molecular circuit to stabilize the interaction between IAA and JA. Combining genetics, genome-wide transcriptome profiling, hormononics and cell biological approaches, we found that MYC2-mediated JA signaling controls the expression of the ETHYLENE RESPONSE FACTOR 115 (ERF115) gene, which is a repressor of ARI. Our genetic data revealed that ERF115-mediated ARI inhibition requires cytokinins (CKs). CKs have long been established as inhibitors of ARI. Altogether, ARI seems to be controlled by a complex molecular network guided by three hormonal pathways (IAA, JA and CK), in which JA-induced ERF115 plays a role of "molecular switch".
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