Title

An SMC-like protein is required for hormogonium motility in the filamentous cyanobacterium Nostoc punctiforme.

Poster Number

05B

Lead Author Major

Biological Sciences

Lead Author Status

Freshman

Second Author Major

Pre-Pharmacy

Second Author Status

Junior

Format

Poster Presentation

Faculty Mentor Name

Douglas Risser

Faculty Mentor Email

drisser@pacific.edu

Faculty Mentor Department

Biological Sciences

Abstract/Artist Statement

Abstract for PURCC 2017

Thomas Harwood & Anthony Trieu

An SMC-like protein is required for hormogonium motility in the filamentous cyanobacterium Nostoc punctiforme.

The goal of this project is to identify the genes controlling hormogonium development and motility in the filamentous cyanobacterium Nostoc punctiforme. N. punctiforme forms nitrogen-fixing endosymbioses with several different plants and fungi. To establish these symbioses, facilitate dispersal, and perform phototaxis, N. punctiforme differentiates into motile filaments, known as hormogonia, capable of gliding motility via a modified type IV pilus-like system. Using a transposon screen, the gene Npun_R5959 was identified as the transposon insertion site in two independent non-motile mutant strains of N. punctiforme. Npun_R5959, encodes a protein that is homologous to SMC (structural maintenance of chromosomes) proteins, which are involved in the organization and segregation of chromosomes during cell division, the regulation of gene expression, and DNA repair. A strain with an in-frame deletion of Npun_R5959 (ΔNpun_R5959) was created to confirm the non-motile phenotype. The resulting strain was non-motile, but differentiated morphologically distinct hormogonia. Results from Western blot analysis imply that Npun_R5959 is dispensable for accumulation of both PilA and HmpD, hormogonium-specific proteins that serve as markers for two independent genetic circuits in the hormogonium gene regulatory network. However, results from immunofluorescence of the extracellular fraction of PilA indicate that PilA is not secreted out of the cell in the ΔNpun_R5959 strain. This phenotype is similar to those reported for previously characterized mutant strains with deletions in certain components of the type IV pilus-like system, and implies that Npun_R5959 may be a component of, or regulate the activity of the gliding motor.

Location

DeRosa University Center, Ballroom

Start Date

29-4-2017 1:00 PM

End Date

29-4-2017 3:00 PM

This document is currently not available here.

Share

COinS
 
Apr 29th, 1:00 PM Apr 29th, 3:00 PM

An SMC-like protein is required for hormogonium motility in the filamentous cyanobacterium Nostoc punctiforme.

DeRosa University Center, Ballroom

Abstract for PURCC 2017

Thomas Harwood & Anthony Trieu

An SMC-like protein is required for hormogonium motility in the filamentous cyanobacterium Nostoc punctiforme.

The goal of this project is to identify the genes controlling hormogonium development and motility in the filamentous cyanobacterium Nostoc punctiforme. N. punctiforme forms nitrogen-fixing endosymbioses with several different plants and fungi. To establish these symbioses, facilitate dispersal, and perform phototaxis, N. punctiforme differentiates into motile filaments, known as hormogonia, capable of gliding motility via a modified type IV pilus-like system. Using a transposon screen, the gene Npun_R5959 was identified as the transposon insertion site in two independent non-motile mutant strains of N. punctiforme. Npun_R5959, encodes a protein that is homologous to SMC (structural maintenance of chromosomes) proteins, which are involved in the organization and segregation of chromosomes during cell division, the regulation of gene expression, and DNA repair. A strain with an in-frame deletion of Npun_R5959 (ΔNpun_R5959) was created to confirm the non-motile phenotype. The resulting strain was non-motile, but differentiated morphologically distinct hormogonia. Results from Western blot analysis imply that Npun_R5959 is dispensable for accumulation of both PilA and HmpD, hormogonium-specific proteins that serve as markers for two independent genetic circuits in the hormogonium gene regulatory network. However, results from immunofluorescence of the extracellular fraction of PilA indicate that PilA is not secreted out of the cell in the ΔNpun_R5959 strain. This phenotype is similar to those reported for previously characterized mutant strains with deletions in certain components of the type IV pilus-like system, and implies that Npun_R5959 may be a component of, or regulate the activity of the gliding motor.