ALBERT

Description: Multiple sclerosis (MS) is a prevalent neurological disease of complex etiology. Here, we describe the characterization of a multi-incident MS family that nominated a rare missense variant (p.G420D) in plasminogen ( PLG ) as a putative genetic risk factor for MS. Genotyping of PLG p.G420D (rs139071351) in 2160 MS patients, and 886 controls from Canada, identified 10 additional probands, two sporadic patients and one control with the variant. Segregation in families harboring the rs139071351 variant, identified p.G420D in 26 out of 30 family members diagnosed with MS, 14 unaffected parents, and 12 out of 30 family members not diagnosed with disease. Despite considerably reduced penetrance, linkage analysis supports cosegregation of PLG p.G420D and disease. Genotyping of PLG p.G420D in 14446 patients, and 8797 controls from Canada, France, Spain, Germany, Belgium, and Austria failed to identify significant association with disease ( P  = 0.117), despite an overall higher prevalence in patients (OR = 1.32; 95% CI = 0.93–1.87). To assess whether additional rare variants have an effect on MS risk, we sequenced PLG in 293 probands, and genotyped all rare variants in cases and controls. This analysis identified nine rare missense variants, and although three of them were exclusively observed in MS patients, segregation does not support pathogenicity. PLG is a plausible biological candidate for MS owing to its involvement in immune system response, blood-brain barrier permeability, and myelin degradation. Moreover, components of its activation cascade have been shown to present increased activity or expression in MS patients compared to controls; further studies are needed to clarify whether PLG is involved in MS susceptibility.

Description: Several variants in strong linkage disequilibrium (LD) at the SP140 locus have been associated with multiple sclerosis (MS), Crohn's disease (CD) and chronic lymphocytic leukemia (CLL). To determine the causal polymorphism, we have integrated high-density data sets of expression quantitative trait loci (eQTL), using GEUVADIS RNA sequences and 1000 Genomes genotypes, with MS-risk variants of the high-density Immunochip array performed by the International Multiple Sclerosis Genetic Consortium (IMSGC). The variants most associated with MS were also correlated with a decreased expression of the full-length RNA isoform of SP140 and an increase of an isoform lacking exon 7. By exon splicing assay, we have demonstrated that the rs28445040 variant was the causal factor for skipping of exon 7. Western blots of peripheral blood mononuclear cells from MS patients showed a significant allele-dependent reduction of the SP140 protein expression. To confirm the association of this functional variant with MS and to compare it with the best-associated variant previously reported by GWAS (rs10201872), a case–control study including 4384 MS patients and 3197 controls was performed. Both variants, in strong LD ( r 2 = 0.93), were found similarly associated with MS [ P -values, odds ratios: 1.9E-9, OR = 1.35 (1.22–1.49) and 4.9E-10, OR = 1.37 (1.24–1.51), respectively]. In conclusion, our data uncover the causal variant for the SP140 locus and the molecular mechanism associated with MS risk. In addition, this study and others previously reported strongly suggest that this functional variant may be shared with other immune-mediated diseases as CD and CLL.

Description: Bacteriophage 29 genome consists of a linear double-stranded DNA with a terminal protein (TP) covalently linked to each 5' end (TP-DNA) that together with a specific sequence constitutes the replication origins. To initiate replication, the DNA polymerase forms a heterodimer with a free TP that recognizes the origins and initiates replication using as primer the hydroxyl group of TP residue Ser232. The 3D structure of the DNA polymerase/TP heterodimer allowed the identification of TP residues that could be responsible for interaction with the DNA polymerase. Here, we examined the role of TP residues Arg158, Arg169, Glu191, Asp198, Tyr250, Glu252, Gln253 and Arg256 by in vitro analyses of mutant derivatives. The results showed that substitution of these residues had an effect on either the stability of the TP/DNA polymerase complex (R158A) or in the functional interaction of the TP at the polymerization active site (R169A, E191A, Y250A, E252A, Q253A and R256A), affecting the first steps of 29 TP-DNA replication. These results allow us to propose a role for these residues in the maintenance of the equilibrium between TP-priming domain stabilization and its gradual exit from the polymerization active site of the DNA polymerase as new DNA is being synthesized.

Description: We present a CO(1–0) survey for cold molecular gas in a representative sample of 13 high- z radio galaxies (HzRGs) at 1.4 〈 z 〈 2.8, using the Australia Telescope Compact Array. We detect CO(1–0) emission associated with five sources: MRC 0114-211, MRC 0152-209, MRC 0156-252, MRC 1138-262 and MRC 2048-272. The CO(1–0) luminosities are in the range $L^{\prime }_{\rm CO} \sim (5\hbox{--}9) \times 10^{10}$ K km s –1 pc 2 . For MRC 0152-209 and MRC 1138-262, part of the CO(1–0) emission coincides with the radio galaxy, while part is spread on scales of tens of kpc and likely associated with galaxy mergers. The molecular gas mass derived for these two systems is M H2  ~ 6 10 10 M ( M H2 / $L^{\prime }_{\rm CO}$  = 0.8). For the remaining three CO-detected sources, the CO(1–0) emission is located in the halo (~50-kpc) environment. These three HzRGs are among the fainter far-IR emitters in our sample, suggesting that similar reservoirs of cold molecular halo gas may have been missed in earlier studies due to pre-selection of IR-bright sources. In all three cases, the CO(1–0) is aligned along the radio axis and found beyond the brightest radio hotspot, in a region devoid of 4.5 μm emission in Spitzer imaging. The CO(1–0) profiles are broad, with velocity widths of ~1000–3600 km s –1 . We discuss several possible scenarios to explain these halo reservoirs of CO(1–0). Following these results, we complement our CO(1–0) study with detections of extended CO from the literature and find at marginal statistical significance (95 per cent level) that CO in HzRGs is preferentially aligned towards the radio jet axis. For the eight sources in which we do not detect CO(1–0), we set realistic upper limits of $L^{\prime }_{\rm CO} \sim 3\hbox{--}4 \times 10^{10}$ K km s –1 pc 2 . Our survey reveals a CO(1–0) detection rate of 38 per cent, allowing us to compare the CO(1–0) content of HzRGs with that of other types of high- z galaxies.

Description: NEXT is an experiment dedicated to neutrinoless double beta decay searches in xenon. The detector is a TPC, holding 100 kg of high-pressure xenon enriched in the 136Xe isotope. It is under construction in the Laboratorio Subterráneo de Canfranc in Spain, and it will begin operations in 2015. The NEXT detector concept provides an energy resolutionbetter than 1% FWHM and a topological signal that can be used to reduce the background. Furthermore, the NEXT technology can be extrapolated to a 1 ton-scale experiment.

Description: A stochastic background of gravitational waves is expected to arise from a superposition of a large number of unresolved gravitational-wave sources of astrophysical and cosmological origin. It should carry unique signatures from the earliest epochs in the evolution of the Universe, inaccessible to standard astrophysical observations. Direct measurements of the amplitude of this background are therefore of fundamental importance for understanding the evolution of the Universe when it was younger than one minute. Here we report limits on the amplitude of the stochastic gravitational-wave background using the data from a two-year science run of the Laser Interferometer Gravitational-wave Observatory (LIGO). Our result constrains the energy density of the stochastic gravitational-wave background normalized by the critical energy density of the Universe, in the frequency band around 100 Hz, to be 〈6.9 x 10(-6) at 95% confidence. The data rule out models of early Universe evolution with relatively large equation-of-state parameter, as well as cosmic (super)string models with relatively small string tension that are favoured in some string theory models. This search for the stochastic background improves on the indirect limits from Big Bang nucleosynthesis and cosmic microwave background at 100 Hz.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉LIGO Scientific Collaboration & Virgo Collaboration -- Abbott, B P -- Abbott, R -- Acernese, F -- Adhikari, R -- Ajith, P -- Allen, B -- Allen, G -- Alshourbagy, M -- Amin, R S -- Anderson, S B -- Anderson, W G -- Antonucci, F -- Aoudia, S -- Arain, M A -- Araya, M -- Armandula, H -- Armor, P -- Arun, K G -- Aso, Y -- Aston, S -- Astone, P -- Aufmuth, P -- Aulbert, C -- Babak, S -- Baker, P -- Ballardin, G -- Ballmer, S -- Barker, C -- Barker, D -- Barone, F -- Barr, B -- Barriga, P -- Barsotti, L -- Barsuglia, M -- Barton, M A -- Bartos, I -- Bassiri, R -- Bastarrika, M -- Bauer, Th S -- Behnke, B -- Beker, M -- Benacquista, M -- Betzwieser, J -- Beyersdorf, P T -- Bigotta, S -- Bilenko, I A -- Billingsley, G -- Birindelli, S -- Biswas, R -- Bizouard, M A -- Black, E -- Blackburn, J K -- Blackburn, L -- Blair, D -- Bland, B -- Boccara, C -- Bodiya, T P -- Bogue, L -- Bondu, F -- Bonelli, L -- Bork, R -- Boschi, V -- Bose, S -- Bosi, L -- Braccini, S -- Bradaschia, C -- Brady, P R -- Braginsky, V B -- Brand, J F J van den -- Brau, J E -- Bridges, D O -- Brillet, A -- Brinkmann, M -- Brisson, V -- Van Den Broeck, C -- Brooks, A F -- Brown, D A -- Brummit, A -- Brunet, G -- Bullington, A -- Bulten, H J -- Buonanno, A -- Burmeister, O -- Buskulic, D -- Byer, R L -- Cadonati, L -- Cagnoli, G -- Calloni, E -- Camp, J B -- Campagna, E -- Cannizzo, J -- Cannon, K C -- Canuel, B -- Cao, J -- Carbognani, F -- Cardenas, L -- Caride, S -- Castaldi, G -- Caudill, S -- Cavaglia, M -- Cavalier, F -- Cavalieri, R -- Cella, G -- Cepeda, C -- Cesarini, E -- Chalermsongsak, T -- Chalkley, E -- Charlton, P -- Chassande-Mottin, E -- Chatterji, S -- Chelkowski, S -- Chen, Y -- Christensen, N -- Chung, C T Y -- Clark, D -- Clark, J -- Clayton, J H -- Cleva, F -- Coccia, E -- Cokelaer, T -- Colacino, C N -- Colas, J -- Colla, A -- Colombini, M -- Conte, R -- Cook, D -- Corbitt, T R C -- Corda, C -- Cornish, N -- Corsi, A -- Coulon, J-P -- Coward, D -- Coyne, D C -- Creighton, J D E -- Creighton, T D -- Cruise, A M -- Culter, R M -- Cumming, A -- Cunningham, L -- Cuoco, E -- Danilishin, S L -- D'Antonio, S -- Danzmann, K -- Dari, A -- Dattilo, V -- Daudert, B -- Davier, M -- Davies, G -- Daw, E J -- Day, R -- De Rosa, R -- Debra, D -- Degallaix, J -- Del Prete, M -- Dergachev, V -- Desai, S -- Desalvo, R -- Dhurandhar, S -- Di Fiore, L -- Di Lieto, A -- Di Paolo Emilio, M -- Di Virgilio, A -- Diaz, M -- Dietz, A -- Donovan, F -- Dooley, K L -- Doomes, E E -- Drago, M -- Drever, R W P -- Dueck, J -- Duke, I -- Dumas, J-C -- Dwyer, J G -- Echols, C -- Edgar, M -- Effler, A -- Ehrens, P -- Ely, G -- Espinoza, E -- Etzel, T -- Evans, M -- Evans, T -- Fafone, V -- Fairhurst, S -- Faltas, Y -- Fan, Y -- Fazi, D -- Fehrmann, H -- Ferrante, I -- Fidecaro, F -- Finn, L S -- Fiori, I -- Flaminio, R -- Flasch, K -- Foley, S -- Forrest, C -- Fotopoulos, N -- Fournier, J-D -- Franc, J -- Franzen, A -- Frasca, S -- Frasconi, F -- Frede, M -- Frei, M -- Frei, Z -- Freise, A -- Frey, R -- Fricke, T -- Fritschel, P -- Frolov, V V -- Fyffe, M -- Galdi, V -- Gammaitoni, L -- Garofoli, J A -- Garufi, F -- Genin, E -- Gennai, A -- Gholami, I -- Giaime, J A -- Giampanis, S -- Giardina, K D -- Giazotto, A -- Goda, K -- Goetz, E -- Goggin, L M -- Gonzalez, G -- Gorodetsky, M L -- Gobler, S -- Gouaty, R -- Granata, M -- Granata, V -- Grant, A -- Gras, S -- Gray, C -- Gray, M -- Greenhalgh, R J S -- Gretarsson, A M -- Greverie, C -- Grimaldi, F -- Grosso, R -- Grote, H -- Grunewald, S -- Guenther, M -- Guidi, G -- Gustafson, E K -- Gustafson, R -- Hage, B -- Hallam, J M -- Hammer, D -- Hammond, G D -- Hanna, C -- Hanson, J -- Harms, J -- Harry, G M -- Harry, I W -- Harstad, E D -- Haughian, K -- Hayama, K -- Heefner, J -- Heitmann, H -- Hello, P -- Heng, I S -- Heptonstall, A -- Hewitson, M -- Hild, S -- Hirose, E -- Hoak, D -- Hodge, K A -- Holt, K -- Hosken, D J -- Hough, J -- Hoyland, D -- Huet, D -- Hughey, B -- Huttner, S H -- Ingram, D R -- Isogai, T -- Ito, M -- Ivanov, A -- Johnson, B -- Johnson, W W -- Jones, D I -- Jones, G -- Jones, R -- Sancho de la Jordana, L -- Ju, L -- Kalmus, P -- Kalogera, V -- Kandhasamy, S -- Kanner, J -- Kasprzyk, D -- Katsavounidis, E -- Kawabe, K -- Kawamura, S -- Kawazoe, F -- Kells, W -- Keppel, D G -- Khalaidovski, A -- Khalili, F Y -- Khan, R -- Khazanov, E -- King, P -- Kissel, J S -- Klimenko, S -- Kokeyama, K -- Kondrashov, V -- Kopparapu, R -- Koranda, S -- Kozak, D -- Krishnan, B -- Kumar, R -- Kwee, P -- La Penna, P -- Lam, P K -- Landry, M -- Lantz, B -- Laval, M -- Lazzarini, A -- Lei, H -- Lei, M -- Leindecker, N -- Leonor, I -- Leroy, N -- Letendre, N -- Li, C -- Lin, H -- Lindquist, P E -- Littenberg, T B -- Lockerbie, N A -- Lodhia, D -- Longo, M -- Lorenzini, M -- Loriette, V -- Lormand, M -- Losurdo, G -- Lu, P -- Lubinski, M -- Lucianetti, A -- Luck, H -- Machenschalk, B -- Macinnis, M -- Mackowski, J-M -- Mageswaran, M -- Mailand, K -- Majorana, E -- Man, N -- Mandel, I -- Mandic, V -- Mantovani, M -- Marchesoni, F -- Marion, F -- Marka, S -- Marka, Z -- Markosyan, A -- Markowitz, J -- Maros, E -- Marque, J -- Martelli, F -- Martin, I W -- Martin, R M -- Marx, J N -- Mason, K -- Masserot, A -- Matichard, F -- Matone, L -- Matzner, R A -- Mavalvala, N -- McCarthy, R -- McClelland, D E -- McGuire, S C -- McHugh, M -- McIntyre, G -- McKechan, D J A -- McKenzie, K -- Mehmet, M -- Melatos, A -- Melissinos, A C -- Mendell, G -- Menendez, D F -- Menzinger, F -- Mercer, R A -- Meshkov, S -- Messenger, C -- Meyer, M S -- Michel, C -- Milano, L -- Miller, J -- Minelli, J -- Minenkov, Y -- Mino, Y -- Mitrofanov, V P -- Mitselmakher, G -- Mittleman, R -- Miyakawa, O -- Moe, B -- Mohan, M -- Mohanty, S D -- Mohapatra, S R P -- Moreau, J -- Moreno, G -- Morgado, N -- Morgia, A -- Morioka, T -- Mors, K -- Mosca, S -- Mossavi, K -- Mours, B -- Mowlowry, C -- Mueller, G -- Muhammad, D -- Muhlen, H Zur -- Mukherjee, S -- Mukhopadhyay, H -- Mullavey, A -- Muller-Ebhardt, H -- Munch, J -- Murray, P G -- Myers, E -- Myers, J -- Nash, T -- Nelson, J -- Neri, I -- Newton, G -- Nishizawa, A -- Nocera, F -- Numata, K -- Ochsner, E -- O'Dell, J -- Ogin, G H -- O'Reilly, B -- O'Shaughnessy, R -- Ottaway, D J -- Ottens, R S -- Overmier, H -- Owen, B J -- Pagliaroli, G -- Palomba, C -- Pan, Y -- Pankow, C -- Paoletti, F -- Papa, M A -- Parameshwaraiah, V -- Pardi, S -- Pasqualetti, A -- Passaquieti, R -- Passuello, D -- Patel, P -- Pedraza, M -- Penn, S -- Perreca, A -- Persichetti, G -- Pichot, M -- Piergiovanni, F -- Pierro, V -- Pinard, L -- Pinto, I M -- Pitkin, M -- Pletsch, H J -- Plissi, M V -- Poggiani, R -- Postiglione, F -- Principe, M -- Prix, R -- Prodi, G A -- Prokhorov, L -- Punken, O -- Punturo, M -- Puppo, P -- Putten, S van der -- Quetschke, V -- Raab, F J -- Rabaste, O -- Rabeling, D S -- Radkins, H -- Raffai, P -- Raics, Z -- Rainer, N -- Rakhmanov, M -- Rapagnani, P -- Raymond, V -- Re, V -- Reed, C M -- Reed, T -- Regimbau, T -- Rehbein, H -- Reid, S -- Reitze, D H -- Ricci, F -- Riesen, R -- Riles, K -- Rivera, B -- Roberts, P -- Robertson, N A -- Robinet, F -- Robinson, C -- Robinson, E L -- Rocchi, A -- Roddy, S -- Rolland, L -- Rollins, J -- Romano, J D -- Romano, R -- Romie, J H -- Rover, C -- Rowan, S -- Rudiger, A -- Ruggi, P -- Russell, P -- Ryan, K -- Sakata, S -- Salemi, F -- Sandberg, V -- Sannibale, V -- Santamaria, L -- Saraf, S -- Sarin, P -- Sassolas, B -- Sathyaprakash, B S -- Sato, S -- Satterthwaite, M -- Saulson, P R -- Savage, R -- Savov, P -- Scanlan, M -- Schilling, R -- Schnabel, R -- Schofield, R -- Schulz, B -- Schutz, B F -- Schwinberg, P -- Scott, J -- Scott, S M -- Searle, A C -- Sears, B -- Seifert, F -- Sellers, D -- Sengupta, A S -- Sentenac, D -- Sergeev, A -- Shapiro, B -- Shawhan, P -- Shoemaker, D H -- Sibley, A -- Siemens, X -- Sigg, D -- Sinha, S -- Sintes, A M -- Slagmolen, B J J -- Slutsky, J -- van der Sluys, M V -- Smith, J R -- Smith, M R -- Smith, N D -- Somiya, K -- Sorazu, B -- Stein, A -- Stein, L C -- Steplewski, S -- Stochino, A -- Stone, R -- Strain, K A -- Strigin, S -- Stroeer, A -- Sturani, R -- Stuver, A L -- Summerscales, T Z -- Sun, K-X -- Sung, M -- Sutton, P J -- Swinkels, B L -- Szokoly, G P -- Talukder, D -- Tang, L -- Tanner, D B -- Tarabrin, S P -- Taylor, J R -- Taylor, R -- Terenzi, R -- Thacker, J -- Thorne, K A -- Thorne, K S -- Thuring, A -- Tokmakov, K V -- Toncelli, A -- Tonelli, M -- Torres, C -- Torrie, C -- Tournefier, E -- Travasso, F -- Traylor, G -- Trias, M -- Trummer, J -- Ugolini, D -- Ulmen, J -- Urbanek, K -- Vahlbruch, H -- Vajente, G -- Vallisneri, M -- Vass, S -- Vaulin, R -- Vavoulidis, M -- Vecchio, A -- Vedovato, G -- van Veggel, A A -- Veitch, J -- Veitch, P -- Veltkamp, C -- Verkindt, D -- Vetrano, F -- Vicere, A -- Villar, A -- Vinet, J-Y -- Vocca, H -- Vorvick, C -- Vyachanin, S P -- Waldman, S J -- Wallace, L -- Ward, H -- Ward, R L -- Was, M -- Weidner, A -- Weinert, M -- Weinstein, A J -- Weiss, R -- Wen, L -- Wen, S -- Wette, K -- Whelan, J T -- Whitcomb, S E -- Whiting, B F -- Wilkinson, C -- Willems, P A -- Williams, H R -- Williams, L -- Willke, B -- Wilmut, I -- Winkelmann, L -- Winkler, W -- Wipf, C C -- Wiseman, A G -- Woan, G -- Wooley, R -- Worden, J -- Wu, W -- Yakushin, I -- Yamamoto, H -- Yan, Z -- Yoshida, S -- Yvert, M -- Zanolin, M -- Zhang, J -- Zhang, L -- Zhao, C -- Zotov, N -- Zucker, M E -- Zweizig, J -- England -- Nature. 2009 Aug 20;460(7258):990-4. doi: 10.1038/nature08278.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Lists of participants and their affiliations appear at the end of the paper.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19693079" target="_blank"〉PubMed〈/a〉

Description: Glycoconjugate vaccines provide effective prophylaxis against bacterial infections. To date, however, no commercial vaccine has been available in which the key carbohydrate antigens are produced synthetically. We describe the large-scale synthesis, pharmaceutical development, and clinical evaluation of a conjugate vaccine composed of a synthetic capsular polysaccharide antigen of Haemophilus influenzae type b (Hib). The vaccine was evaluated in clinical trials in Cuba and showed long-term protective antibody titers that compared favorably to licensed products prepared with the Hib polysaccharide extracted from bacteria. This demonstrates that access to synthetic complex carbohydrate-based vaccines is feasible and provides a basis for further development of similar approaches for other human pathogens.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Verez-Bencomo, V -- Fernandez-Santana, V -- Hardy, Eugenio -- Toledo, Maria E -- Rodriguez, Maria C -- Heynngnezz, Lazaro -- Rodriguez, Arlene -- Baly, Alberto -- Herrera, Luis -- Izquierdo, Mabel -- Villar, Annette -- Valdes, Yury -- Cosme, Karelia -- Deler, Mercedes L -- Montane, Manuel -- Garcia, Ernesto -- Ramos, Alexis -- Aguilar, Aristides -- Medina, Ernesto -- Torano, Gilda -- Sosa, Ivan -- Hernandez, Ibis -- Martinez, Raydel -- Muzachio, Alexis -- Carmenates, Ania -- Costa, Lourdes -- Cardoso, Felix -- Campa, Concepcion -- Diaz, Manuel -- Roy, Rene -- New York, N.Y. -- Science. 2004 Jul 23;305(5683):522-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for the Study of Synthetic Antigens, Facultad de Quimica, Universidad de la Habana, Ciudad Habana, Cuba, 10400. vicente@fq.uh.cu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15273395" target="_blank"〉PubMed〈/a〉

Description: Corals belong to the most basal class of the Phylum Cnidaria, which is considered the sister group of bilaterian animals, and thus have become an emerging model to study the evolution of developmental mechanisms. Although cell renewal, differentiation, and maintenance of pluripotency are cellular events shared by multicellular animals, the cellular basis of these fundamental biological processes are still poorly understood. To understand how changes in gene expression regulate morphogenetic transitions at the base of the eumetazoa, we performed quantitative RNA-seq analysis during Acropora digitifera ’s development. We collected embryonic, larval, and adult samples to characterize stage-specific transcription profiles, as well as broad expression patterns. Transcription profiles reconstructed development revealing two main expression clusters. The first cluster grouped blastula and gastrula and the second grouped subsequent developmental time points. Consistently, we observed clear differences in gene expression between early and late developmental transitions, with higher numbers of differentially expressed genes and fold changes around gastrulation. Furthermore, we identified three coexpression clusters that represented discrete gene expression patterns. During early transitions, transcriptional networks seemed to regulate cellular fate and morphogenesis of the larval body. In late transitions, these networks seemed to play important roles preparing planulae for switch in lifestyle and regulation of adult processes. Although developmental progression in A. digitifera is regulated to some extent by differential coexpression of well-defined gene networks, stage-specific transcription profiles appear to be independent entities. While negative regulation of transcription is predominant in early development, cell differentiation was upregulated in larval and adult stages.