Additive interactions between the moon snail Euspira heros and the sea star Asterias forbesi , two predators of the surfclam Spisula solidissima

Oecologia ◽  
1999 ◽  
Vol 119 (3) ◽  
pp. 461-466 ◽  
Author(s):  
Eric J. Weissberger
1979 ◽  
Vol 78 (1) ◽  
pp. 59-75
Author(s):  
DAVID J. PRIOR ◽  
ANNE M. SCHNEIDERMAN ◽  
SHARON I. GREENE

1. The evasive jump response of Spisula can be elicited by contact of the siphons with the tube feet of a starfish (Asterias forbesi). 2. The level of responsiveness varies with the size of the individual clam; small clams (2.0-5.0 cm) being very responsive, large clams (12.0-18.0 cm) being totally unresponsive. 3. The cell bodies of touch-sensitive neurones subserving the siphons are located in the visceral ganglion. The mean area of the receptive fields of these neurones in small clams is 33.8 mm2 and in large clams is 9.7 mm2. 4. In small clams the large proportion of the total siphon surface innervated by single touch-sensitive neurones results in considerable overlap of receptive fields. As a result of this overlap, numerous touch-sensitive neurones are activated by a point stimulus. 5. The variation in jump responsiveness of large and small clams is correlated with the size of the receptive fields of touch-sensitive neurones. Note: Present address: Department of Zoology, University of California, Berkeley, CA 04720. Present address: Boston University Marine Program, Woods Hole, MA 02543.


2015 ◽  
Vol 160 (9) ◽  
pp. 2349-2351 ◽  
Author(s):  
Elizabeth Fahsbender ◽  
Ian Hewson ◽  
Karyna Rosario ◽  
Allison D. Tuttle ◽  
Arvind Varsani ◽  
...  

1990 ◽  
Vol 14 (1) ◽  
pp. 19-30 ◽  
Author(s):  
L.A. Leonard ◽  
J.D. Strandberg ◽  
J.A. Winkelstein
Keyword(s):  
Sea Star ◽  

1984 ◽  
Vol 52 (01) ◽  
pp. 001-003 ◽  
Author(s):  
J A Marcum ◽  
J Levin ◽  
R A Prendergast

SummaryClotting enzyme activity was detected in lysates prepared from the coelomocytes of Asterias forbesi following incubation with endotoxin-activated Limulus amebocyte lysate. This activity was not detected in the cell-free coelomic fluid. The enzymatic activity from the sea star lysate hydrolyzed the synthetic substrate S2222 but not S2238 or S2251, and polymerized partially purified Limulus clottable protein. The clotting enzyme activity was not detected following treatment of the sea star cell lysate with endotoxin or with the clotting enzyme from Limulus lysate. The enzymatic activity, generated in sea star cell lysate by the activated Limulus lysate, was inhibited by the addition of benzamidine; and its effect was suppressed with rabbit anti-sera directed against Asterias whole cell lysate, but not with anti-sera directed against the previously reported Sea Star Factor.


2019 ◽  
Author(s):  
Elliot W. Jackson ◽  
Charles Pepe-Ranney ◽  
Mitchell R. Johnson ◽  
Daniel L. Distel ◽  
Ian Hewson

AbstractViral metagenomes prepared from tissues from Forbes’ sea star (Asterias forbesi) led to the discovery of a complete genome of a novel sea star densovirus (AfaDV). The genome organization of AfaDV and phylogenetic analysis place this virus among the Ambidensovirus genus in the subfamily Densoviridae, family Parvoviridae. AfaDV shares 78% nucleotide pairwise identity to the sea star associated densovirus (SSaDV), previously described as the putative causative agent of Sea Star Wasting Syndrome among sea stars from the Northwest Pacific. SSaDV was not found in specimens collected in this study, and the discovery of AfaDV might explain previous reports of SSaDV among sea stars from the Atlantic Coast. A qPCR assay was designed to assess tissue tropism, host specificity, and prevalence of AfaDV among wild populations of sea stars at five locations on the North American Atlantic Coast. AfaDV was detected in all three common sea star species (Asterias forbesi, Asterias rubens, and Henricia sp.) found in the region and was highly prevalent (80-100% of individuals tested, n=134), among populations collected at disparate sites 7 years apart. AfaDV was detected in the body wall, gonads, and pyloric caeca (digestive gland) of specimens but was not detected in their coelomic fluid. A significant difference in viral load was found between tissue types with the pyloric caeca having the highest viral load suggesting it is the primary site of viral replication in the animal. Further investigation of Asterias forbesi gonad tissue found germline cells (oocytes) to be virus positive suggesting a potential route of vertical transmission. Taken together, these observations show that the presence AfaDV is not an indicator of Sea Star Wasting Syndrome because AfaDV is a common constituent of these animals’ microbiome, regardless of health. These results broaden the understanding of echinoderm densoviruses outside the context of disease that suggest these viruses might form commensal or mutualistic relationships with their hosts.


2020 ◽  
Vol 86 (6) ◽  
Author(s):  
Elliot W. Jackson ◽  
Charles Pepe-Ranney ◽  
Mitchell R. Johnson ◽  
Daniel L. Distel ◽  
Ian Hewson

ABSTRACT The etiology of sea star wasting syndrome is hypothesized to be caused by a densovirus, sea star-associated densovirus (SSaDV), that has previously been reported on the Pacific and Atlantic Coasts of the United States. In this study, we reevaluated the presence of SSaDV among sea stars from the North American Atlantic Coast and in doing so discovered a novel densovirus that we have named Asterias forbesi-associated densovirus (AfaDV), which shares 78% nucleotide pairwise identity with SSaDV. In contrast to previous studies, SSaDV was not detected in sea stars from the North American Atlantic Coast. Using a variety of PCR-based techniques, we investigated the tissue tropism, host specificity, and prevalence of AfaDV among populations of sea stars at five locations along the Atlantic Coast. AfaDV was detected in three sea star species (Asterias forbesi, Asterias rubens, and Henricia sp.) found in this region and was highly prevalent (>80% of individuals tested; n = 134), among sampled populations. AfaDV was detected in the body wall, gonads, and pyloric caeca (digestive gland) of specimens but was not detected in their coelomic fluid. A significant difference in viral load (copies mg−1) was found between tissue types, with the pyloric caeca having the highest viral loads. Further investigation of Asterias forbesi gonad tissue found germ line cells (oocytes) to be virus positive, suggesting a potential route of vertical transmission. Taken together, these observations show that the presence of AfaDV is not an indicator of sea star wasting syndrome because AfaDV is a common constituent of these animals’ microbiome, regardless of health. IMPORTANCE Sea star wasting syndrome is a disease primarily observed on the Pacific and Atlantic Coasts of North America that has significantly impacted sea star populations. The etiology of this disease is unknown, although it is hypothesized to be caused by a densovirus, SSaDV. However, previous studies have not found a correlation between SSaDV and sea star wasting syndrome on the North American Atlantic Coast. This study suggests that this observation may be explained by the presence of a genetically similar densovirus, AfaDV, that may have confounded previous studies. SSaDV was not present in sea stars screened in this study, and instead, AfaDV was commonly found in sea star populations across the New England region, with no apparent signs of disease. These results suggest that sea star densoviruses may be common constituents of the animals’ microbiome, and the diversity and extent of these viruses among wild populations may be greater than previously recognized.


PLoS ONE ◽  
2017 ◽  
Vol 12 (12) ◽  
pp. e0188523 ◽  
Author(s):  
Caitlin Bucci ◽  
Madison Francoeur ◽  
Jillon McGreal ◽  
Roxanna Smolowitz ◽  
Vanesa Zazueta-Novoa ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document