Biology Reference
In-Depth Information
PatS and HetN appear to act consecutively at establishing and maintenance
of the spatial pattern of heterocyst distribution after perception of N stress.
A gradient of HetR, dependent on PatS and HetN, has been estimated to
take place in the filaments with concentration decreasing in proximity to
the heterocysts, and it has been proposed that diffusion of PatS- and HetN-
derived signals promote HetR degradation close to the (pro)heterocysts
(
Risser & Callahan, 2009
). It is conceivable that PatS (or a derivative of PatS
and HetN) binds HetR inhibiting HetR interaction with DNA and mark-
ing it for degradation, with the effect of hampering differentiation of (pro)
heterocyst neighboring cells. Nonetheless, the expression of
hetR
is well doc-
umented to increase in the cells differentiating into heterocysts (
Black, Cai,
& Wolk, 1993
;
Toyoshima et al., 2010
). Molecular details of PatS and HetN
processing and intercellular transfer, as well as of the HetR post-translational
regulation, are missing.
4.4.2. Other elements influencing heterocyst distribution
The
patA
gene encodes a protein with a C-terminal CheY-like phospho-
acceptor domain and an N-terminal PATAN domain possibly involved in
protein-protein interactions (
Liang, Scarpino, & Haselkorn, 1992
;
Makarova,
Koonin, Haselkorn, & Galperin, 2006
), and
patL
encodes a pentapeptide
repeat protein (
Liu & Wolk, 2011
). Inactivation of any of them produces
heterocysts mostly located at the filament ends, and PatA and PatL may
interact with each other (
Liu & Wolk, 2011
). In the case of
patA
, this phe-
notype has been reported to be abolished by inactivation of
patS
and
hetN
,
thus implicating PatA in attenuation of the negative signals derived first
from PatS and later from HetN (
Orozco, Risser, & Callahan, 2006
).
The
hefF
gene encodes a putative cysteine-dependent protease, and its
mutants show aberrant cell morphology, lack heterocysts and exhibit increased
levels of the HetR protein both in the presence and absence of combined
nitrogen, but decreased activation of some tested HetR-dependent genes or
promoters (
Risser & Callahan, 2008
;
Wong & Meeks, 2001
). Overexpres-
sion of
hetF
produces an Mch phenotype and induction of the
hetR
gene
in all cells of the filament, and it compensates the effect of deletion of the
patA
gene (
Risser & Callahan, 2008
;
Wong & Meeks, 2001
). Thus HetF, on
which PatA may have a positive effect, appears to be involved in regulation
of the HetR levels, both in vegetative cells and heterocysts, as well as of its
transcriptional activity (
Risser & Callahan, 2008
;
Wong & Meeks, 2001
).
However, HetF would not be required for establishment of the HetR
gradients promoted by PatS and HetN signals (
Risser & Callahan, 2009
).
