Grant: Discovery Grants Program - Individual
University of New Brunswick
$43,000.00
Cellular stress responses in the evolution of multicellular complexity
EF 2018-19
Résumé
Our research program addresses one of the most challenging topics in evolutionary biology - the evolution of complexity. The emergence of new levels of complexity in multicellular lineages was contingent on the evolution of non-reproductive (somatic) cells. However, despite its significance, the mechanistic basis for the evolution of soma is not well understood in any lineage. To address this important question, we are using a group of green algae (the Volvocales) that comprises both unicellular (e.g, Chlamydomonas) and multicellular species (e.g., Volvox) with various levels of complexity. In Volvox carteri, a single gene - regA - is necessary and sufficient to establish the somatic cell fate. We have previously hypothesized that the evolution of soma involved the co-option of pathways that allow unicellular organisms to adaptively respond to various stress factors by investing in survival at a cost to immediate reproduction. The general objective of this research is to elucidate the mechanistic basis for the co-option of stress responses into developmental pathways during the evolution of multicellularity in Volvocales. Specifically, we want to address how the developmental regulation of regA might have evolved. We will pursue several complementary objectives and methodological approaches. (i) Identify upstream components of the signal transduction pathway associated with the induction of regA during environmental stress. (ii) Test if these signals/pathways are also involved in the developmentally-regulated induction of regA. (iii) Identify regulatory elements responsible for regA expression using bioinformatics and a yeast one-hybrid system (to probe for potential interactions between the predicted regulatory sequences and their postulated binding factors). The proposed research provides a new framework to address the evolution of soma and multicellular complexity based on the co-option of pre-existing responses to stress. This research also address several other important topics, including the contribution of cis-regulatory elements to the evolution of morphological traits, the mechanism(s) underlying gene co-option and functional diversification, and how differences in cell size translate into differential gene expression.*
Programme
Discovery Grants Program - Individual
Bénéficiaire
Emplacement
New Brunswick, Canada
Type de bénéficiaire
Academia
Type
Grant
Source
NSERC's Awards Data
Tel que publié
Application id
222935-2013
Name nom
Nedelcu, Aurora
Department département
Biology (Fredericton)
Organization id
75
Institution établissement
University of New Brunswick
Province en
New Brunswick
Province fr
Nouveau-Brunswick
Country en
CANADA
Country fr
CANADA
Fiscal year exercice financier
2018
Competition year année de concours
2013
Award amount
43000
Program id
RGPIN
Program name en
Discovery Grants Program - Individual
Program name fr
Programme de subventions à la découverte - individuelles
Group en
Discovery grants programs
Group fr
Programmes de subventions à la découverte
Committee code
1501
Committee name en
Genes, Cells and Molecules
Committee name fr
Gènes, cellules et molécules
Area of application code
1200
Area of application group en
Advancement of knowledge
Area of application group fr
Avancement des connaissances
Area of application en
Advancement of knowledge
Area of application fr
Avancement des connaissances
Research subject code
5005
Research subject group en
Genetics
Research subject group fr
Génétique
Research subject en
Evolutionary genetics
Research subject fr
Génétique évolutive
Partie
5
Nb partie
5
Application title
Cellular stress responses in the evolution of multicellular complexity
Keyword
NSERC
Application summary
Our research program addresses one of the most challenging topics in evolutionary biology - the evolution of complexity. The emergence of new levels of complexity in multicellular lineages was contingent on the evolution of non-reproductive (somatic) cells. However, despite its significance, the mechanistic basis for the evolution of soma is not well understood in any lineage. To address this important question, we are using a group of green algae (the Volvocales) that comprises both unicellular (e.g, Chlamydomonas) and multicellular species (e.g., Volvox) with various levels of complexity. In Volvox carteri, a single gene - regA - is necessary and sufficient to establish the somatic cell fate. We have previously hypothesized that the evolution of soma involved the co-option of pathways that allow unicellular organisms to adaptively respond to various stress factors by investing in survival at a cost to immediate reproduction. The general objective of this research is to elucidate the mechanistic basis for the co-option of stress responses into developmental pathways during the evolution of multicellularity in Volvocales. Specifically, we want to address how the developmental regulation of regA might have evolved. We will pursue several complementary objectives and methodological approaches. (i) Identify upstream components of the signal transduction pathway associated with the induction of regA during environmental stress. (ii) Test if these signals/pathways are also involved in the developmentally-regulated induction of regA. (iii) Identify regulatory elements responsible for regA expression using bioinformatics and a yeast one-hybrid system (to probe for potential interactions between the predicted regulatory sequences and their postulated binding factors). The proposed research provides a new framework to address the evolution of soma and multicellular complexity based on the co-option of pre-existing responses to stress. This research also address several other important topics, including the contribution of cis-regulatory elements to the evolution of morphological traits, the mechanism(s) underlying gene co-option and functional diversification, and how differences in cell size translate into differential gene expression.*