Characterization of Npun_3825 : A Hybrid Histidine Kinase/Response Regulator
Poster Number
04B
Format
Poster Presentation
Faculty Mentor Name
Douglas Risser
Faculty Mentor Department
Biological Sciences
Abstract/Artist Statement
The goal of this project is to identify the genes essential for hormogonium development and motility in the filamentous cyanobacterium Nostoc punctiforme. N. punctiforme differentiates hormogonia, motile filaments that can establish nitrogen-fixing symbioses with plants and fungi, and perform phototaxis. Hormogonium motility is driven by a modified type IV pilus-like system that may also secrete a polysaccharide essential for motility. As part of an ongoing project to identify the genes essential for hormogonium development and motility in N. punctiforme, we are performing an in depth analysis of Npun_R3825, one of several genes identified as essential for hormogonium motility using a transposon mutagenesis screen. Npun_R3825 encodes a hybrid histidine kinase/response regulator, a type of protein that plays a role in signal transduction, allowing bacteria to sense and respond to their environment by activating a phosphorelay. In order to elucidate the role that Npun_R3825 plays in the gene-signaling cascade controlling hormogonium development, a strain with an in-frame deletion of Npun_R3825 was created. This strain was non-motile and failed to undergo any of the morphological changes associated with the development of hormogonia. The gene regulatory network controlling hormogonium development has two independent pathways, one promoting transcription of the type IV pilus system component pilA and the other promoting transcription of the chemotaxis system component hmpD. Western blot analysis of PilA and HmpD indicated that neither of these hormogonium-specific proteins was upregulated upon induction in the Npun_R3825 mutant strain. Secretion of hormogonium polysaccharide was also completely abolished in the absence of Npun_R3825. Collectively, these results demonstrate that all known markers of hormogonium development are lost in the Npun_R3825 mutant strain. It is hypothesized that Npun_3825 may function as the master regulator that initiates the hormogonium gene regulatory network.
Location
DeRosa University Center, Ballroom
Start Date
29-4-2017 1:00 PM
End Date
29-4-2017 3:00 PM
Characterization of Npun_3825 : A Hybrid Histidine Kinase/Response Regulator
DeRosa University Center, Ballroom
The goal of this project is to identify the genes essential for hormogonium development and motility in the filamentous cyanobacterium Nostoc punctiforme. N. punctiforme differentiates hormogonia, motile filaments that can establish nitrogen-fixing symbioses with plants and fungi, and perform phototaxis. Hormogonium motility is driven by a modified type IV pilus-like system that may also secrete a polysaccharide essential for motility. As part of an ongoing project to identify the genes essential for hormogonium development and motility in N. punctiforme, we are performing an in depth analysis of Npun_R3825, one of several genes identified as essential for hormogonium motility using a transposon mutagenesis screen. Npun_R3825 encodes a hybrid histidine kinase/response regulator, a type of protein that plays a role in signal transduction, allowing bacteria to sense and respond to their environment by activating a phosphorelay. In order to elucidate the role that Npun_R3825 plays in the gene-signaling cascade controlling hormogonium development, a strain with an in-frame deletion of Npun_R3825 was created. This strain was non-motile and failed to undergo any of the morphological changes associated with the development of hormogonia. The gene regulatory network controlling hormogonium development has two independent pathways, one promoting transcription of the type IV pilus system component pilA and the other promoting transcription of the chemotaxis system component hmpD. Western blot analysis of PilA and HmpD indicated that neither of these hormogonium-specific proteins was upregulated upon induction in the Npun_R3825 mutant strain. Secretion of hormogonium polysaccharide was also completely abolished in the absence of Npun_R3825. Collectively, these results demonstrate that all known markers of hormogonium development are lost in the Npun_R3825 mutant strain. It is hypothesized that Npun_3825 may function as the master regulator that initiates the hormogonium gene regulatory network.