39 research outputs found
Sediments and herbivory as sensitive indicators of coral reef degradation
No full text© 2016 by the author(s). Around the world, the decreasing health of coral reef ecosystems has highlighted the need to better understand the processes of reef degradation. The development of more sensitive tools, which complement traditional methods of monitoring coral reefs, may reveal earlier signs of degradation and provide an opportunity for pre-emptive responses. We identify new, sensitive metrics of ecosystem processes and benthic composition that allow us to quantify subtle, yet destabilizing, changes in the ecosystem state of an inshore coral reef on the Great Barrier Reef. Following severe climatic disturbances over the period 2011-2012, the herbivorous reef fish community of the reef did not change in terms of biomass or functional groups present. However, fish-based ecosystem processes showed marked changes, with grazing by herbivorous fishes declining by over 90%. On the benthos, algal turf lengths in the epilithic algal matrix increased more than 50% while benthic sediment loads increased 37-fold. The profound changes in processes, despite no visible change in ecosystem state, i.e., no shift to macroalgal dominance, suggest that although the reef has not undergone a visible regime-shift, the ecosystem is highly unstable, and may sit on an ecological knife-edge. Sensitive, process-based metrics of ecosystem state, such as grazing or browsing rates thus appear to be effective in detecting subtle signs of degradation and may be critical in identifying ecosystems at risk for the future
Cirrhilabrus apterygia Tea & Allen & Goatley & Gill & Frable 2021, new combination
No full textCirrhilabrus apterygia (Allen, 1983), new combination Connie’s Wrasse Other names: Mutant Wrasse; Rowley Shoals Wrasse Figures 1, 2A–B, 2E–F, 3A, 4B; Table 1. Conniella apterygia Allen 1983 (Holotype WAM P.27659-006; type locality Bedwell Island, Clerke Reef, Rowley Shoals, Western Australia): Allen & Russell 1986 (checklist; Rowley Shoals, Scott Reef, and Seringapatam Reef).–– Allen & Steene 1987: 151, pl 87-1 (colour photograph).–– Parenti & Randall 2000 (annotated checklist of labroid fishes).–– Hoese et al. 2006 (checklist; Zoological Catalogue of Australia).–– Kuiter 2010: 154 (colour photographs A–F; specimens photographed from Rowley Shoals).–– Allen 2018: 211, pl 74-14 (illustration).— Parenti & Randall 2018 (annotated checklist of labroid fishes).–– Swainston 2020: 630 (checklist of Australian labrid species).–– Tea et al. 2021b (included as part of a phylogenomic study of Cirrhilabrus). Diagnosis. A species of Cirrhilabrus distinguished from all other congeners based on the following combination of colouration and morphological characters: absence of pelvic fins and pelvic girdle; lateral line with 21–26 pored scales (16–17 in the dorsoanterior series, 5–9 in the posterior peduncular series); caudal fin rhomboidal to lanceolate in males; both sexes with eight to ten stripes, purple in life and in preservation; preopercle purple in preservation. Description. Dorsal-fin rays XI,9 (one specimen with X,9); all soft rays branched except first ray unbranched (one specimen with first ray branched); anal-fin rays III,9; all soft rays branched except first ray unbranched; last dorsal and anal-fin ray branched to base; pectoral-fin rays 15 (one specimen with 15/13), upper two unbranched; principal caudal-fin rays 7+6, uppermost and lowermost unbranched; upper procurrent caudal-fin rays 6, lower procurrent caudal-fin rays 6; lateral line interrupted, with dorsoanterior series of pored scales 17 (16–17) and midlateral posterior peduncular series 9 (5–9); first pored scale on posterior peduncular series often pitted; last pored scale on posterior peduncular series enlarged and overlapping hypural crease; scales above lateral line to origin of dorsal fin 2; scales below lateral line to origin of anal fin 6; median predorsal scales 5; rows of scales on cheek 2; circumpeduncular scales 16; gill rakers 7 (6–7) + 9 (9–11) = 16 (15–18); pseudobranchial filaments 12 (10–12); vertebrae 9+16; epineurals 12 (Fig. 4B). Body moderately elongate and compressed, depth 3.6 (3.2–3.8) in SL, width 2.2 (2.0–2.5) in depth; head length (HL) 3.1 (3.0–3.5) in SL; snout pointed, its length 4.3 (3.2–3.9) in HL; orbit diameter 3.8 (3.0–3.6) in HL; depth of caudal peduncle 2.1 (2.0–2.4) in HL. Mouth small, terminal, and oblique, with maxilla almost reaching vertical at front edge of orbit; dentition typical of the genus with three pairs of canine teeth present anteriorly at side of upper jaw, first forward-projecting, next two strongly recurved and outcurved, third longest; an irregular row of very small conical teeth medial to upper canines; lower jaw with a single stout pair of canines anteriorly which protrude obliquely outward and are slightly lateral to medial pair of upper jaw; no teeth on roof of mouth. Posterior margin of preoperculum with 44/45 (32–45) very fine serrations; margins of posterior and ventral edges of preoperculum free to about level of middle pupil. Anterior nostril in short membranous tube, located nearer to orbit than snout tip; posterior nostril larger, roughly ovoid to rectangular, located just medial and anterior to upper edge of eye. Scales cycloid; head scaled except snout and interorbital space; 6 (6–7) large scales on opercle; a broad naked zone on membranous edge of preopercle; a row of large, elongate, pointed scales along base of dorsal fin, one per element, scales progressively shorter posteriorly on soft portion of fin; anal fin with a similar basal row of scales; last pored scale of lateral line (posterior to hypural plate) enlarged and pointed; one scale above and below last pored scale also enlarged; pectoral fins naked except for a few small scales at fleshy base. Origin of dorsal fin above second or third lateral-line scale, predorsal length 3.0 (2.7–3.2) in SL; first 1–5 dorsal-fin spines progressively longer, sixth to ninth subequal, 10th to 11th longest, 2.5 (2.5–3.4) in HL; interspinous membranes of dorsal fin in males extend beyond dorsal-fin spines, with each membrane extending in a pointed cirrus beyond spine; 8th to 9th dorsal-fin soft ray longest, 1.8 (1.7–2.5) in HL, remaining rays progressively shorter; origin of anal fin below base of 9th dorsal-fin spine; third anal-fin spine longest, 2.9 (1.7–2.5) in HL; interspinous membranes of anal fin extended as on dorsal fin; anal-fin soft rays relatively uniform in length, 7th to 9th longest, 1.5 (1.4–2.2) in HL; dorsal- and anal-fin rays just reaching past caudal-fin base; caudal fin of males rhomboidal to lanceolate; pectoral fins short, reaching vertical between bases of 6th or 7th dorsal-fin spines, longest ray 1.5 (1.4–1.5) in HL; pelvic fins and pelvic girdle. Colouration of males in life. Based on colour photographs of specimens when freshly dead, and photos of live individuals taken in the field (Figs. 1A–C, 2A–B, & 3A): head orange-purple above, often magenta washed, abruptly white to cream below lower limit of orbit; interorbital region and nape orange-red, with four to five thin white lines from just above nostrils to dorsal-fin origin; lavender stripe present from lower edge of maxilla to anterior orbit; iris lavender, with orange ring around pupil; distal edge of orbit yellow; lower margin of cheek to outer margin of preopercle bright purple; interopercle purple; operculum white, broadly edged posteriorly with a reddish purple bar, connecting ventrally with oblique reddish purple wedge over pectoral-fin base; body cream to pale yellow above, gradually lightening to white ventrally; body with eight to ten bright purple stripes, first six starting a short distance behind reddish purple opercular and pectoral-fin markings, so as to form an intervening white wedge of similar width; remaining stripes originating from lower edge of opercle and isthmus; all stripes terminate at base of caudal fin, except ventralmost two to three stripes terminating at anal-fin origin; dorsal fin translucent yellow; anterior spinous dorsal fin with two submarginal, parallel yellow stripes breaking into indistinct spots and short stripes toward soft dorsal fin; outermost margin of dorsal fin narrowly bright blue; scales at base of dorsal fin magenta to fuchsia; caudal fin translucent pink to yellow with a pair of prominent blue chevrons converging at caudal-fin terminus, central region often with yellow and blue spots and short stripes; anal fin similar to dorsal fin; pectoral fins translucent pink, distal edge more strongly coloured. Colouration of females and juveniles in life. Based on colour photographs of specimens when freshly dead, and photos of live individuals taken in the field (Fig. 1B–D): similar to males, except bars and stripes on body less pronounced, and body colouration pinkish; caudal fins of females rounded or weakly rhomboidal and without blue chevron markings; distal edge of caudal peduncle with a very small black spot. Colouration in alcohol. Based on colour photographs of preserved specimens (Fig. 2E–F): similar to life, except body uniformly tan; several osseous elements remain purple, including purple scale markings on body, median-fin spines and rays, infraorbitals, maxilla, premaxilla, dentary, anguloarticular, and preopercle; black spot on distal edge of caudal peduncle in females and juveniles remains. Habitat and distribution. Cirrhilabrus apterygia occurs on offshore reefs off northwestern Western Australia, including Rowley Shoals, Scott, and Seringapatam Reefs. ROV dive footage from the RV Falkor’s Australian Mesophotic Coral Exploration cruise indicates that the species also occurs on Ashmore Reef, 840 km west of Darwin, Northern Territory. It frequents rubble bottoms covered with macroalgae cover at depths between 20–60m, but also occurs in mesophotic coral ecosystems as deep as 140 m. Etymology. Allen (1983) named the species apterygia, meaning “without fins,” in reference to the distinctive lack of pelvic fins and associated elements. To be treated as a noun in apposition. We retain the use of Connie’s Wrasse as the preferred common name, after Connie Lagos Allen, wife of the second author, for whom the junior synonym Conniella was named. The species is also commonly referred to as the mutant wrasse, alluding to its atypical pelvic morphology, as well as the eponymous Rowley Shoals Wrasse, after its type locality. Material examined. Cirrhilabrus apterygia: WAM P. 27659-006 (holotype), 55.1 mm SL, male, outer reef slope east of Bedwell Island, Clerke Reef, Rowley Shoals, Western Australia, 32 m, 22 July 1982 (Fig. 2E); WAM P.27668-003 (paratype), 57.7 mm SL, male, same data as holotype except collected at 35 m, 27 July 1982 (Fig. 2F); WAM P.27668-015 (paratype), 31.2 mm SL, female, same data as male paratype (specimen cleared and stained; Fig. 4B); WAM P.28036-003, 54.5 mm SL, male, Clerke Reef, outer reef 1 km off southern tip of Bedwell Island, Rowley Shoals, Western Australia, 20–35 m, 13 August 1983; WAM P.28037-006, 47.3 mm SL, male, same data as WAM P.28036-003 except collected at 45–50 m, 14 August 1983; NMV A 29675 -009, 54.9 mm SL, male, Cunningham Island, Imperieuse Reef, Rowley Shoals, Western Australia, 108–140 m, 16 June 2007; NVM A 29675 - 010, 3 specimens, 45.0– 52.3 mm SL, two males and one female, same data as NVM A 29675 -009. Cirrhilabrus earlei: ZRC 60866, 69.4 mm SL, male, Marshall Islands, Micronesia (Fig. 2G); CAS 213114 (paratype), 56.5 mm SL, male, Augulpelu Reef, Palau (Fig. 2H). Cirrhilabrus rubrimarginatus: AMS I. 45300.288, 43.8 mm SL, (specimen cleared and stained; Fig. 4A). Cirrhilabrus naokoae: AMS I. 45300.513, 49.1 mm SL, (specimen cleared and stained). Paracheilinus lineopunctatus: AMS I. 45300.194, 51.0 mm SL, (specimen cleared and stained; Fig. 4C). Paracheilinus mccoskeri: AMS I. 45300.185, 5 specimens, 31.0– 54.5 mm SL, (specimens cleared and stained). Pseudocheilinus ocellatus: AMS I. 45300.485, 48.8 mm SL, (specimen cleared and stained). Pseudocheilinops ataenia: AMS I. 45300.056, 2 specimens, 24.1–34.7 mm SL (specimen cleared and stained). Pteragogus flagellifera: AMS I. 187755-034, 52.0 mm SL, (specimen cleared and stained).Published as part of Tea, Yi-Kai, Allen, Gerald R., Goatley, Christopher H. R., Gill, Anthony C. & Frable, Benjamin W., 2021, Redescription of Conniella apterygia Allen and its reassignment in the genus Cirrhilabrus Temminck and Schlegel (Teleostei: Labridae), with comments on cirrhilabrin pelvic morphology, pp. 493-509 in Zootaxa 5061 (3) on pages 495-499, DOI: 10.11646/zootaxa.5061.3.5, http://zenodo.org/record/564993
Processing and Localization of the African Swine Fever Virus CD2v Transmembrane Protein
No full textABSTRACT
The African swine fever virus (ASFV)-encoded CD2v transmembrane protein is required for the hemadsorption of red blood cells around infected cells and is also required for the inhibition of bystander lymphocyte proliferation in response to mitogens. We studied the expression of CD2v by expressing the gene with a V5 tag downstream from the signal peptide near the N terminus and a hemagglutinin (HA) tag at the C terminus. In ASFV-infected cells, a full-length glycosylated form of the CD2v protein, which migrated mainly as a 89-kDa product, was detected, as well as an N-terminal glycosylated fragment of 63 kDa and a C-terminal nonglycosylated fragment of 26 kDa. All of these forms of the protein were localized in the membrane fraction of cells. The 26-kDa C-terminal fragment was also produced in infected cells treated with brefeldin A. These data indicate that the CD2v protein is cleaved within the luminal domain and that this occurs in the endoplasmic reticulum or Golgi compartments. Confocal microscopy showed that most of the expressed CD2v protein was localized within cells rather than at the cell surface. Comparison of the localization of full-length CD2v with that of a deletion mutant lacking all of the cytoplasmic tail apart from the 12 membrane-proximal amino acids indicated that signals within the cytoplasmic tail are responsible for the predominant localization of the full-length and C-terminal 26-kDa fragment within membranes around the virus factories, which contain markers for the Golgi compartment. Processing of the CD2v protein was not observed in uninfected cells, indicating that it is induced by ASFV infection.</jats:p
Role of African Swine Fever Virus Proteins EP153R and EP402R in Reducing Viral Persistence in Blood and Virulence in Pigs Infected with BeninΔDP148R
No full text19 Pág.This research was funded by Biotechnology and Biological Sciences Research Council, grant number BBS/E/I/00007039/7031/7034 with support by the Pirbright flow cytometry and sequencing facilities. Some parts of the quoted research were funded in part by UK Aid from the UK Government through Global Alliance for Livestock Veterinary Medicines (GALVmed) (grant number and FCDO. The findings and conclusions contained within are those of the authors and do not necessarily reflect positions or policies of GALVmed.Peer reviewe
Differential Effect of Deleting Members of African Swine Fever Virus Multigene Families 360 and 505 from the Genotype II Georgia 2007/1 Isolate on Virus Replication, Virulence, and Induction of Protection
No full text21 Pàg.African swine fever virus multigene family (MGF) 360 and 505 genes have roles in suppressing the type I interferon response and in virulence in pigs. The role of the individual genes is poorly understood. Different combinations of these genes were deleted from the virulent genotype II Georgia 2007/1 isolate. Deletion of five copies of MGF 360 genes, MGF360-10L, -11L, -12L, -13L, and -14L, and three copies of MGF505-1R, -2R, and -3R reduced virus replication in macrophages and attenuated virus in pigs. However, only 25% of the immunized pigs were protected against challenge. Deletion of MGF360-12L, -13L, and -14L and MGF505-1R in combination with a negative serology marker, K145R (GeorgiaΔK145RΔMGF(A)), reduced virus replication in macrophages and virulence in pigs, since no clinical signs or virus genome in blood were observed following immunization. Four of six pigs were protected after challenge. In contrast, deletion of MGF360-13L and -14L, MGF505-2R and -3R, and K145R (GeorgiaΔK145RΔMGF(B)) did not reduce virus replication in macrophages. Following immunization of pigs, clinical signs were delayed, but all pigs reached the humane endpoint. Deletion of genes MGF360-12L, MGF505-1R, and K145R reduced replication in macrophages and attenuated virulence in pigs since no clinical signs or virus genome in blood were observed following immunization. Thus, the deletion of MGF360-12L and MGF505-1R, in combination with K145R, was sufficient to dramatically attenuate virus infection in pigs. However, only two of six pigs were protected, suggesting that deletion of additional MGF genes is required to induce a protective immune response. Deletion of MGF360-12L, but not MGF505-1R, from the GeorgiaΔK145R virus reduced virus replication in macrophages, indicating that MGF360-12L was most critical for maintaining high levels of virus replication in macrophages. IMPORTANCE African swine fever has a high socioeconomic impact and no vaccines to aid control. The African swine fever virus (ASFV) has many genes that inhibit the host's interferon response. These include related genes that are grouped into multigene families, including MGF360 and 505. Here, we investigated which MGF360 and 505 genes were most important for viral attenuation and protection against genotype II strains circulating in Europe and Asia. We compared viruses with deletions of MGF genes. Deletion of just two MGF genes in combination with a third gene, K145R, a possible marker for vaccination, is sufficient for virus attenuation in pigs. Deletion of additional MGF360 genes was required to induce higher levels of protection. Furthermore, we showed that the deletion of MGF360-12L, combined with K145R, impairs virus replication in macrophages in culture. Our results have important implications for understanding the roles of the ASFV MGF genes and for vaccine development.We acknowledge funding from BBSRC Grant numbers BBS/E/1/00007039, 7031,
7038 and 7034 and support from the Pirbright flow cytometry and sequencing facilitiesPeer reviewe
A study of the impact of perceived individual stigma, social stigma and social support on treatment seeking behaviors of victims of sexual exploitation in Georgia, 2012
No full textThe issue of commercial sexual exploitation of children (CSEC) is a growing problem within the United States of America. According to research by Report of the Special Rapporteur on the Sale of Children, Child Prostitution, and Child Pornography, 300,000 CSEC children may live within the United States every year (United Nations Economic and Social Council, 1996). Other research by the National Center for Missing and Exploited Children (1999) has estimated that the number of CSEC children may be increasing to around 300,000-500,000 per year. Research is lacking in providing more current statistics regarding the number of children being commercially sexually exploited due to the clandestine nature of the lifestyle. The CSEC population is described as an intricate network of pimps, johns, and child victims (Slavin, 2002; Dalla, Xia, & Kennedy, 2003; Gragg, Petta, Berstein, Eisen, & Quinn, 2007). The population is often created of children that are deemed homeless, thrownaways, or transient/migrant (Gragg, Petta, Berstein, Eisen, & Quinn, 2007) or have not been reported missing by those with guardianship. According to research by A Future Not A Past, a national organization to end child prostitution, most CSEC children enter the Life around 12-13 years of age (A Future Not A Past, 2009). This dissertation examines the impact of perceived individual stigma, perceived social stigma and social supports impact on treatment seeking behavior among victims of CSEC. Through a mixed methods study, fifty (50) participants were selected through snowball sampling to participate in the quantitative research agenda and ten (10) participated in in-depth interviews. The findings showed that 48% reported seeking treatment for CSEC and 76% stated they had strong social support systems. The qualitative analysis supported the position that victims of CSEC will seek treatment with the help of strong social support systems
Deletion of the K145R and DP148R Genes from the Virulent ASFV Georgia 2007/1 Isolate Delays the Onset, but Does Not Reduce Severity, of Clinical Signs in Infected Pigs
No full textAfrican swine fever virus causes a frequently fatal disease of domestic pigs and wild boar that has a high economic impact across 3 continents. The large double-stranded DNA genome codes for approximately 160 proteins. Many of these have unknown functions and this hinders our understanding of the virus and host interactions. The purpose of the study was to evaluate the role of two virus proteins, K145R and DP148R, in virus replication in macrophages and virulence in pigs. To do this, the DP148R gene, alone or in combination with the K145R gene, was deleted from the virulent genotype II Georgia 2007/1 isolate. Neither of these deletions reduced the ability of the viruses to replicate in porcine macrophages compared to the parental wild-type virus. Pigs infected with GeorgiaΔDP148R developed clinical and post-mortem signs and high viremia, typical of acute African swine fever, and were culled on day 6 post-infection. The additional deletion of the K145R gene delayed the onset of clinical signs and viremia in pigs by 3 days, but pigs showed signs of acute African swine fever and were culled on days 10 or 13 post-infection. The results show that the deletion of DP148R did not attenuate the genotype II Georgia 2007/1 isolate, contrary to the results obtained with the genotype I Benin97/1 isolate. Additional deletion of the K145R gene delayed clinical signs, but infected pigs reached the humane endpoint. The deletion of additional genes would be required to attenuate the virus
The transcriptomic insight into the differential susceptibility of African Swine Fever in inbred pigs
No full textAbstract African swine fever (ASF) is a global threat to animal health and food security. ASF is typically controlled by strict biosecurity, rapid diagnosis, and culling of affected herds. Much progress has been made in developing modified live virus vaccines against ASF. There is host variation in response to ASF infection in the field and under controlled conditions. To better understand the dynamics underlying this host differential morbidity, whole transcriptome profiling was carried out in twelve immunized and five sham immunized pigs. Seventeen MHC homozygous inbred Large white Babraham pigs were sampled at three time points before and after the challenge. The changes in the transcriptome profiles of infected animals were surveyed over time. In addition, the immunization effect on the host response was studied as well among the contrasts of all protection subgroups. The results showed two promising candidate genes to distinguish between recovered and non-recovered pigs after infection with a virulent African swine fever virus (ASFV) pre-infection: HTRA3 and GFPT2 (padj < 0.05). Variant calling on the transcriptome assemblies showed a two-base pair insertion into the ACOX3 gene closely located to HTRA3 that may regulate its expression as a putative genomic variant for ASF. Several significant DGEs, enriched gene ontology (GO) terms, and KEGG pathways at 1 day and 7 days post-infection, compared to the pre-infection, indicate a significant inflammation response immediately after ASF infection. The presence of the virus was confirmed by the mapping of RNA-Seq reads on two whole viral genome sequences. This was concordant with a higher virus load in the non-recovered animals 7 days post-infection. There was no transcriptome signature on the immunization at pre-infection and 1 day post-infection. More samples and data from additional clinical trials may support these findings
Identification of residues within the African swine fever virus DP71L protein required for dephosphorylation of translation initiation factor eIF2α and inhibiting activation of pro-apoptotic CHOP
No full text
