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Role of the CRK family in regulation of gravitropic responses in Arabidopsis

TÉMAKIÍRÁS

Intézmény: Szegedi Tudományegyetem
biológiai tudományok
Biológia Doktori Iskola

témavezető: Cséplő Ágnes
társ-témavezető: Szabados László
helyszín (magyar oldal): HAS, Plant Biology Institute, Arabidopsis Molecular and Genetic Group
helyszín rövidítés: SzBK


A kutatási téma leírása:

Plants depend on roots which anchore them to soil, facilitate water and nutrient uptake. Roots are sensing different environmental stimuli, such as gravity, soil composition including salinity or water shortage. Adequate response to such effects is vital for plants, and needs to be studied to be able to develop breeding strategies for tolerating suboptimal conditions. Extreme environmental conditions such as drought, high soil salinity or nutrient deprivation cause phenotypic alterations in plant roots. Root architecture was recently shown to affect drought avoidance in crops. Despite of extensive research on regulatory pathways controlling responses to environmental stimuli, little is known about the way how these stimuli affect root development. The CDPK-SnRK superfamily consists of seven types of serine-threonine protein kinases. including the Ca2+/calmodulin-dependent kinase-related kinase (CRK) subfamily. CRK5 is one of the eight members of Arabidopsis CRK subfamily. We have recently showed that the plasmamembrane localized CRK5 is required for proper polar localization of PIN2 in Arabidopsis roots. Inactivation of CRK5 causes root gravitropic defect, reduced root growth and enhanced lateral root formation. PIN2 is depleted from apical membranes of epidermal cells and shows mixed apolar and apical localization in the cortex of the crk5 mutant. CRK5 phosphorylates the hydrophilic T-loop of PIN2, suggesting that it plays a role in the regulation of PIN2 membrane recycling. Auxin is depleted from the root tips of crk5 mutant by enhanced auxin flow through the cortex towards the elongation zone. CRK5 phosphorylates the hydrophilic T-loop of PIN2, suggesting that it plays a role in the regulation of PIN2 membrane recycling. Our preliminary results also suggest that CRK5 might regulate signaling through reactive oxygen and nitrogen species, as H2O2 and NO levels were altered in crk5 mutant roots. It is intriguing that CRK5 might be a novel player of ROS signal transduction in roots.

General aim of the project is the understanding the structure and function of developmental and stress-related regulatory networks controlled by the Ca2+/calmodulin-dependent kinase-related kinase (CRK) family, to acquire information on the function of CRK-controlled signal transduction, how it controls auxin signaling, root development and geotropic responses. We would like to get deeper insight how CRK5 is involved in ROS signal transduction, whether this kinase family has influence on responses to salt and oxidative stress. Our recent research includes the verification the function of the eight CRK protein kinase family members, the analysis of the T-DNA insertion mutants of CRK family member genes and transgenic lines overexpressing CRK protein as well as the characterization of developmental alterations, studying the roles in gravitropic processes either in roots or stems and in responses to salt and oxidative stresses. As an alternative program, we plan to study the phosphorylation targets of CRK5 and identify its phosphorylation sites in PIN2 and other substrates. Additionally, the study the function of PIN2 phosphorylation via altering target sites by in vitro mutagenesis will also be considered. We would also like to identify the CRK5-interacting proteins and protein complexes. Understanding the CRK5-controlled signaling and regulatory pathways regulated by reactive oxygen species (ROS) during osmotic (salt) and oxidative (peroxide) stresses are in progress.

előírt nyelvtudás: angol
további elvárások: 
basic level of molecular biology technics

felvehető hallgatók száma: 1

Jelentkezési határidő: 2015-10-13


2024. IV. 17.
ODT ülés
Az ODT következő ülésére 2024. június 14-én, pénteken 10.00 órakor kerül sor a Semmelweis Egyetem Szenátusi termében (Bp. Üllői út 26. I. emelet).

 
Minden jog fenntartva © 2007, Országos Doktori Tanács - a doktori adatbázis nyilvántartási száma az adatvédelmi biztosnál: 02003/0001. Program verzió: 2.2358 ( 2017. X. 31. )