scholarly journals Coordinating the morphogenesis-differentiation balance by tweaking the cytokinin-gibberellin equilibrium

PLoS Genetics ◽  
2021 ◽  
Vol 17 (4) ◽  
pp. e1009537
Author(s):  
Alon Israeli ◽  
Yogev Burko ◽  
Sharona Shleizer-Burko ◽  
Iris Daphne Zelnik ◽  
Noa Sela ◽  
...  

Morphogenesis and differentiation are important stages in organ development and shape determination. However, how they are balanced and tuned during development is not fully understood. In the compound leaved tomato, an extended morphogenesis phase allows for the initiation of leaflets, resulting in the compound form. Maintaining a prolonged morphogenetic phase in early stages of compound-leaf development in tomato is dependent on delayed activity of several factors that promote differentiation, including the CIN-TCP transcription factor (TF) LA, the MYB TF CLAU and the plant hormone Gibberellin (GA), as well as on the morphogenesis-promoting activity of the plant hormone cytokinin (CK). Here, we investigated the genetic regulation of the morphogenesis-differentiation balance by studying the relationship between LA, CLAU, TKN2, CK and GA. Our genetic and molecular examination suggest that LA is expressed earlier and more broadly than CLAU and determines the developmental context of CLAU activity. Genetic interaction analysis indicates that LA and CLAU likely promote differentiation in parallel genetic pathways. These pathways converge downstream on tuning the balance between CK and GA. Comprehensive transcriptomic analyses support the genetic data and provide insights into the broader molecular basis of differentiation and morphogenesis processes in plants.

2020 ◽  
Author(s):  
Alon Israeli ◽  
Yogev Burko ◽  
Sharona Shleizer-Burko ◽  
Iris Daphne Zelnik ◽  
Noa Sela ◽  
...  

AbstractMorphogenesis and differentiation are important stages in organ development and shape determination. However, how they are balanced and tuned during development is not fully understood. In the compound leaved tomato, an extended morphogenesis phase allows for the initiation of leaflets, resulting in the compound form. Maintaining a prolonged morphogenetic phase in early stages of compound-leaf development is dependent on delayed activity of several factors that promote differentiation, including CIN-TCP transcription factor (TF) LA, the MYB TF CLAU and the plant hormone Gibberellin (GA). Here, we investigated the genetic regulation of the morphogenesis-differentiation balance by studying the relationship between LA, CLAU and GA. Our genetic and molecular examination suggest that LA is expressed more broadly than CLAU and determines the spatio-temporal context of CLAU activity. We demonstrate that both LA and CLAU affect the Cytokinin/Gibberellin (CK/GA) balance. LA reduces the sensitivity of the leaf margin to CK, shown before to be also affected by CLAU. CLAU affects leaf active GA content and sensitivity, shown previously to be also influenced by LA. Therefore, LA and CLAU likely function in parallel pathways to promote leaf differentiation by converging on common downstream processes, including the CK/GA balance.


eLife ◽  
2018 ◽  
Vol 7 ◽  
Author(s):  
Emi Ito ◽  
Kazuo Ebine ◽  
Seung-won Choi ◽  
Sakura Ichinose ◽  
Tomohiro Uemura ◽  
...  

RAB5 is a key regulator of endosomal functions in eukaryotic cells. Plants possess two different RAB5 groups, canonical and plant-unique types, which act via unknown counteracting mechanisms. Here, we identified an effector molecule of the plant-unique RAB5 in Arabidopsis thaliana, ARA6, which we designated PLANT-UNIQUE RAB5 EFFECTOR 2 (PUF2). Preferential colocalization with canonical RAB5 on endosomes and genetic interaction analysis indicated that PUF2 coordinates vacuolar transport with canonical RAB5, although PUF2 was identified as an effector of ARA6. Competitive binding of PUF2 with GTP-bound ARA6 and GDP-bound canonical RAB5, together interacting with the shared activating factor VPS9a, showed that ARA6 negatively regulates canonical RAB5-mediated vacuolar transport by titrating PUF2 and VPS9a. These results suggest a unique and unprecedented function for a RAB effector involving the integration of two RAB groups to orchestrate endosomal trafficking in plant cells.


BioEssays ◽  
2014 ◽  
Vol 36 (7) ◽  
pp. 706-713 ◽  
Author(s):  
Hannes Braberg ◽  
Erica A. Moehle ◽  
Michael Shales ◽  
Christine Guthrie ◽  
Nevan J. Krogan

2018 ◽  
Vol 20 (2) ◽  
pp. 624-637 ◽  
Author(s):  
Mengyun Wu ◽  
Shuangge Ma

2017 ◽  
Vol 31 (2) ◽  
pp. 184-196 ◽  
Author(s):  
Sida Liao ◽  
Teresa Davoli ◽  
Yumei Leng ◽  
Mamie Z. Li ◽  
Qikai Xu ◽  
...  

2021 ◽  
Vol 3 (12) ◽  
Author(s):  
Viola Halder ◽  
Brianna McDonnell ◽  
Rebecca Shapiro

Candida albicans is an opportunistic fungal pathogen found in the oral mucosa, the gut, the vaginal mucosa, and humans' skin. While C. albicans can cause superficial infections, severe invasive infections can occur in immunocompromised individuals. Understanding the survival mechanisms and pathogenesis of C. albicans is critical for novel antifungal drug discovery. Determining the relationships between different genes can create a genetic interaction map, which can identify complementary gene sets, central to C. albicans survival, as potential drug targets in combination therapy. A genetic approach using the CRISPR-Cas9-based genome editing platform will focus on genetic interaction analysis of C. albicans stress response genes. The ultimate goal is to create a stress response gene deletion library to study its pathogen survival role. This library of single and double stress response gene mutants will be screened under diverse growth conditions to assess their relative fitness. Genetic interaction analysis will help map out epistatic interactions between fungal genes involved in growth, survival, and pathogenesis and uncover putative targets for combination antifungal therapy based on negative or synthetic lethal genetic interactions.


2021 ◽  
Vol 4 (1) ◽  
Author(s):  
Connor P. O’Meara ◽  
Lucia Guerri ◽  
Divine-Fondzenyuy Lawir ◽  
Fernando Mateos ◽  
Mary Iconomou ◽  
...  

AbstractTo capture the global gene network regulating the differentiation of immature T cells in an unbiased manner, large-scale forward genetic screens in zebrafish were conducted and combined with genetic interaction analysis. After ENU mutagenesis, genetic lesions associated with failure of T cell development were identified by meiotic recombination mapping, positional cloning, and whole genome sequencing. Recessive genetic variants in 33 genes were identified and confirmed as causative by additional experiments. The mutations affected T cell development but did not perturb the development of an unrelated cell type, growth hormone-expressing somatotrophs, providing an important measure of cell-type specificity of the genetic variants. The structure of the genetic network encompassing the identified components was established by a subsequent genetic interaction analysis, which identified many instances of positive (alleviating) and negative (synthetic) genetic interactions. Several examples of synthetic lethality were subsequently phenocopied using combinations of small molecule inhibitors. These drugs not only interfered with normal T cell development, but also elicited remission in a model of T cell acute lymphoblastic leukaemia. Our findings illustrate how genetic interaction data obtained in the context of entire organisms can be exploited for targeted interference with specific cell types and their malignant derivatives.


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