ORCID Profile
0000-0002-5946-9060
Current Organisations
University of Canterbury
,
University of Helsinki
,
Biology Centre CAS
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Publisher: Springer Science and Business Media LLC
Date: 15-02-2019
DOI: 10.1038/S42003-018-0274-5
Abstract: Abiotic and biotic factors control ecosystem bio ersity, but their relative contributions remain unclear. The ultraoligotrophic ecosystem of the Antarctic Dry Valleys, a simple yet highly heterogeneous ecosystem, is a natural laboratory well-suited for resolving the abiotic and biotic controls of community structure. We undertook a multidisciplinary investigation to capture ecologically relevant biotic and abiotic attributes of more than 500 sites in the Dry Valleys, encompassing observed landscape heterogeneities across more than 200 km 2 . Using richness of autotrophic and heterotrophic taxa as a proxy for functional complexity, we linked measured variables in a parsimonious yet comprehensive structural equation model that explained significant variations in biological complexity and identified landscape-scale and fine-scale abiotic factors as the primary drivers of ersity. However, the inclusion of linkages among functional groups was essential for constructing the best-fitting model. Our findings support the notion that biotic interactions make crucial contributions even in an extremely simple ecosystem.
Publisher: Elsevier BV
Date: 05-2023
Publisher: Wiley
Date: 07-2020
DOI: 10.1002/PLD3.248
Publisher: Cold Spring Harbor Laboratory
Date: 03-08-2023
DOI: 10.1101/2023.08.02.551742
Abstract: Cellular responses to abiotic stress involve multiple secondary messengers including reactive oxygen species (ROS), Ca 2+ , phytohormones such as abscisic acid (ABA) and chloroplast-to-nucleus retrograde signals such as 3’-phosphoadenosine 5’-phosphate (PAP). Mechanism(s) by which these messengers, produced in different subcellular compartments, intersect for cell regulation remain enigmatic. Here we demonstrate a mechanistic link enabling ABA and the chloroplast retrograde signal PAP to coordinate both chloroplast and plasma membrane ROS production. In whole leaves, PAP alters various ROS-related processes including plasmodesmal permeability as well as responses to ozone and the bacterial elicitor flg22, but largely quenches ROS during oxidative stress. Conversely, in guard cells, both PAP and ABA induce a ROS burst in both chloroplasts via photosynthetic electron transport, and the apoplast via the RESPIRATORY BURST OXIDASE HOMOLOG (RBOH). Both subcellular ROS sources were necessary for ABA- and PAP-mediated stomatal closure. However, PAP signaling erges from ABA by activating RBOHD, instead of RBOHF, for apoplastic ROS production. We identify calcium-dependent protein kinases (CPKs) transcriptionally induced by PAP as the post-translational activators of RBOHD-mediated ROS production. CPK13, CPK32, and CPK34 concurrently activate RBOHD and the slow anion channel SLAC1 by phosphorylating two Serine (S) residues, including S120 which is also targeted by the core ABA signaling kinase OPEN STOMATA 1 (OST1). Consequently, overexpressing the PAP-induced CPKs rescues stomatal closure in ost1. Our data identify chloroplasts, as sources and mediators of ROS and retrograde signals such PAP, to be critical environmental sensors and focal node in the multifaceted cellular stress response network. The chloroplast is an important node to coordinate multiple plant signaling pathways in response to stresses such as drought. However, how does it function in specialized cells for which carbon fixation is secondary? Here we show that the chloroplast retrograde signal 3’-phosphoadenosine 5’-phosphate (PAP) plays multiple roles in reactive oxygen species (ROS) signaling and homeostasis. While PAP suppresses ROS in photosynthetic tissue, surprisingly PAP induces ROS in chloroplasts and extracellular space of guard cells to induce stomatal closure. We decipher how PAP-induced proteins activate both extracellular ROS production and anion channels for stomatal closure, thus providing a mechanism by which chloroplasts provide a strategic complement to canonical hormonal pathways in regulating plant physiological responses in specialized cells.
No related grants have been discovered for Michael Wrzaczek.