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Intercellular Signaling Activity Encoded by hetN in the Cyanobacterium Anabaena sp. strain PCC 7120.
|Title:||Intercellular Signaling Activity Encoded by hetN in the Cyanobacterium Anabaena sp. strain PCC 7120.|
|Authors:||Rivers, Orion S.|
|Date Issued:||Aug 2017|
|Publisher:||University of Hawaiʻi at Mānoa|
|Abstract:||Developmental regulators coordinate cellular differentiation in many organisms.|
Regulators can be small molecules or proteins. Developmental regulators called morphogens are
produced in source cell(s) that determine the developmental fate of cells adjacent to the source in
a concentration dependent manner. The filamentous cyanobacterium Anabaena sp. Strain PCC
7120 is a model organism used to study cellular differentiation. When Anabaena filaments are
supplied a source of fixed nitrogen a single cell type, vegetative cells, comprise the filaments.
However, removal of fixed nitrogen from the medium induces differentiation of one in every 10-
15 cells into a heterocyst. Heterocysts are terminally differentiated cells that are the sites of
atmospheric nitrogen fixation. Differentiation within Anabaena requires 24 hours and can be
divided into four stages: induction, patterning, commitment, and morphogenesis. The periodic
pattern of heterocyst is initially determined by the interplay of HetR, the primary activator of
differentiation within Anabaena, and PatS, a diffusible inhibitor expressed during the patterning
stage. The initial pattern of heterocysts in maintained during growth by a secondary inhibitor,
HetN, which is expressed in mature heterocysts. The pentapeptide sequence RGSGR is
conserved in the amino acid sequences of both inhibitors and has been shown to inhibit
differentiation and induce HetR degradation when added to the medium, bind directly to HetR in
vitro, and is required for the inhibitory function of PatS. In this work HetN was found to require
the RGSGR sequence for inhibitory function and did not require predicted ketoacyl reductase
activity. Full-length HetN was found to be confined to source cell(s) membranes, but a hetNdependent
inhibitory signal was shown to move away from source heterocysts in a manner
similar to a paracrine-type intercellular signal. The hetN-dependent inhibitory signal was found
not to require the intercellular channel forming protein SepJ. However, mutation of sepJ reduced
the signal range of the HetN-dependent inhibitory signal, suggesting its involvement in signal
transport. Finally, evidence supporting the use of M119 of HetN as the developmentally
regulated translational start site is presented. This work contributes to our knowledge of
morphogen signals and supports the role of HetN as an inhibitory morphogen within Anabaena.
|Description:||Ph.D. Thesis. University of Hawaiʻi at Mānoa 2017.|
|Rights:||All UHM dissertations and theses are protected by copyright. They may be viewed from this source for any purpose, but reproduction or distribution in any format is prohibited without written permission from the copyright owner.|
|Appears in Collections:||
Ph.D. - Microbiology|
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