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Structure and signaling at hydroid polyp-stolon junctions, revisited.

Harmata KL, Somova EL, Parrin AP, Bross LS, Glockling SL, Blackstone NW - Biol Open (2015)

Bottom Line: Transmission electron microscopy identified mitochondrion-rich cells adjacent to a thick layer of mesoglea at polyp-stolon junctions.The myonemes of these myoepithelial cells extend from the thickened mesoglea to the rigid perisarc on the outside of the colony.The perisarc thus anchors the myoepithelial cells and allows them to pull against the mesoglea and open the lumen of the polyp-stolon junction, while relaxation of these cells closes the lumen.

View Article: PubMed Central - PubMed

Affiliation: Department of Biological Sciences, Northern Illinois University, DeKalb, IL 60115, USA.

No MeSH data available.


Related in: MedlinePlus

A hypothesis for how gastrovascular flow is regulated in colonial hydroids. At the polyp-stolon junctions there are mitochondrion-rich myoepithelial cells (MRCs) and valve-like structures; these valves in part regulate the flow (Blackstone et al., 2004a,b). Additional regulation may be provided by myoepithelial contractions of the polyps and possibly the stolons.
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BIO012187F1: A hypothesis for how gastrovascular flow is regulated in colonial hydroids. At the polyp-stolon junctions there are mitochondrion-rich myoepithelial cells (MRCs) and valve-like structures; these valves in part regulate the flow (Blackstone et al., 2004a,b). Additional regulation may be provided by myoepithelial contractions of the polyps and possibly the stolons.

Mentions: Recently discovered mitochondrion-rich myoepithelial cells at the junction of polyps and stolons may have a central role in regulating the patterns of gastrovascular flow in a colony (Fig. 1). These cells may operate a valve-like structure at the polyp-stolon junction (Blackstone et al., 2004a,b). The existence of such valves explains a variety of observations, including the delay between feeding and the circulation of food-containing gastrovascular fluid from the polyps (Dudgeon et al., 1999). Further, the large numbers of mitochondria in these cells suggest that operating these valves is metabolically demanding. In animal cells, biogenesis of mitochondria is thought to be regulated by PGC-1α (peroxisome proliferator-activated receptor-γ coactivator-1α). PGC-1α is a potent metabolic sensor and regulator (Wu et al., 1999; Cunningham et al., 2007; Arany et al., 2008). In response to a high level of metabolic demand indicated by a low ATP/ADP ratio and low to moderate reactive oxygen species (ROS), PGC-1α will initiate mitochondrial biogenesis. This suggests that any metazoan cell that is subject to intense metabolic demand will become mitochondrion-rich. Indeed, such cells are found in human organs with high metabolism (e.g. brain, heart, and kidney). Salt glands of marine birds and the gills of some fish also exhibit mitochondrion-rich cells (Chance et al., 1964; Evans et al., 2005; Hiroi et al., 2005).Fig. 1.


Structure and signaling at hydroid polyp-stolon junctions, revisited.

Harmata KL, Somova EL, Parrin AP, Bross LS, Glockling SL, Blackstone NW - Biol Open (2015)

A hypothesis for how gastrovascular flow is regulated in colonial hydroids. At the polyp-stolon junctions there are mitochondrion-rich myoepithelial cells (MRCs) and valve-like structures; these valves in part regulate the flow (Blackstone et al., 2004a,b). Additional regulation may be provided by myoepithelial contractions of the polyps and possibly the stolons.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4582120&req=5

BIO012187F1: A hypothesis for how gastrovascular flow is regulated in colonial hydroids. At the polyp-stolon junctions there are mitochondrion-rich myoepithelial cells (MRCs) and valve-like structures; these valves in part regulate the flow (Blackstone et al., 2004a,b). Additional regulation may be provided by myoepithelial contractions of the polyps and possibly the stolons.
Mentions: Recently discovered mitochondrion-rich myoepithelial cells at the junction of polyps and stolons may have a central role in regulating the patterns of gastrovascular flow in a colony (Fig. 1). These cells may operate a valve-like structure at the polyp-stolon junction (Blackstone et al., 2004a,b). The existence of such valves explains a variety of observations, including the delay between feeding and the circulation of food-containing gastrovascular fluid from the polyps (Dudgeon et al., 1999). Further, the large numbers of mitochondria in these cells suggest that operating these valves is metabolically demanding. In animal cells, biogenesis of mitochondria is thought to be regulated by PGC-1α (peroxisome proliferator-activated receptor-γ coactivator-1α). PGC-1α is a potent metabolic sensor and regulator (Wu et al., 1999; Cunningham et al., 2007; Arany et al., 2008). In response to a high level of metabolic demand indicated by a low ATP/ADP ratio and low to moderate reactive oxygen species (ROS), PGC-1α will initiate mitochondrial biogenesis. This suggests that any metazoan cell that is subject to intense metabolic demand will become mitochondrion-rich. Indeed, such cells are found in human organs with high metabolism (e.g. brain, heart, and kidney). Salt glands of marine birds and the gills of some fish also exhibit mitochondrion-rich cells (Chance et al., 1964; Evans et al., 2005; Hiroi et al., 2005).Fig. 1.

Bottom Line: Transmission electron microscopy identified mitochondrion-rich cells adjacent to a thick layer of mesoglea at polyp-stolon junctions.The myonemes of these myoepithelial cells extend from the thickened mesoglea to the rigid perisarc on the outside of the colony.The perisarc thus anchors the myoepithelial cells and allows them to pull against the mesoglea and open the lumen of the polyp-stolon junction, while relaxation of these cells closes the lumen.

View Article: PubMed Central - PubMed

Affiliation: Department of Biological Sciences, Northern Illinois University, DeKalb, IL 60115, USA.

No MeSH data available.


Related in: MedlinePlus