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1. Electrostatic sheathing of lipoprotein lipase is essential for its movement across capillary endothelial cells

Author

Song, Wenxin, Beigneux, Anne P, Winther, Anne-Marie L, Kristensen, Kristian K, Grønnemose, Anne L, Yang, Ye, Tu, Yiping, Munguia, Priscilla, Morales, Jazmin, Jung, Hyesoo, de Jong, Pieter J, Jung, Cris J, Miyashita, Kazuya, Kimura, Takao, Nakajima, Katsuyuki, Murakami, Masami, Birrane, Gabriel, Jiang, Haibo, Tontonoz, Peter, Ploug, Michael, Fong, Loren G, and Young, Stephen G

Subjects
Animals, Capillaries, Endothelial Cells, Lipoprotein Lipase, Mice, Receptors, Lipoprotein, Static Electricity, Lipoproteins, Metabolism, Medical and Health Sciences, Immunology
Abstract

GPIHBP1, an endothelial cell (EC) protein, captures lipoprotein lipase (LPL) within the interstitial spaces (where it is secreted by myocytes and adipocytes) and transports it across ECs to its site of action in the capillary lumen. GPIHBP1's 3-fingered LU domain is required for LPL binding, but the function of its acidic domain (AD) has remained unclear. We created mutant mice lacking the AD and found severe hypertriglyceridemia. As expected, the mutant GPIHBP1 retained the capacity to bind LPL. Unexpectedly, however, most of the GPIHBP1 and LPL in the mutant mice was located on the abluminal surface of ECs (explaining the hypertriglyceridemia). The GPIHBP1-bound LPL was trapped on the abluminal surface of ECs by electrostatic interactions between the large basic patch on the surface of LPL and negatively charged heparan sulfate proteoglycans (HSPGs) on the surface of ECs. GPIHBP1 trafficking across ECs in the mutant mice was normalized by disrupting LPL-HSPG electrostatic interactions with either heparin or an AD peptide. Thus, GPIHBP1's AD plays a crucial function in plasma triglyceride metabolism; it sheathes LPL's basic patch on the abluminal surface of ECs, thereby preventing LPL-HSPG interactions and freeing GPIHBP1-LPL complexes to move across ECs to the capillary lumen.

Published
2022

2. Deficiency in ZMPSTE24 and resulting farnesyl–prelamin A accumulation only modestly affect mouse adipose tissue stores[S]

Author

Heizer, Patrick J, Yang, Ye, Tu, Yiping, Kim, Paul H, Chen, Natalie Y, Hu, Yan, Yoshinaga, Yuko, de Jong, Pieter J, Vergnes, Laurent, Morales, Jazmin E, Li, Robert L, Jackson, Nicholas, Reue, Karen, Young, Stephen G, and Fong, Loren G

Subjects
Biological Sciences, Medical Physiology, Biomedical and Clinical Sciences, 2.1 Biological and endogenous factors, Metabolic and endocrine, Adipose Tissue, Alleles, Animals, Cell Nucleus, Female, Lamin Type A, Male, Membrane Proteins, Metalloendopeptidases, Mice, Mice, Knockout, Mice, Transgenic, animal models, farnesylation, nuclear lamins, fluorescence microscopy, lipodystrophies, zinc metallopeptidase STE24, Biochemistry and Cell Biology, Medical Biochemistry and Metabolomics, Biochemistry & Molecular Biology, Biochemistry and cell biology, Medical biochemistry and metabolomics
Abstract

Zinc metallopeptidase STE24 (ZMPSTE24) is essential for the conversion of farnesyl-prelamin A to mature lamin A, a key component of the nuclear lamina. In the absence of ZMPSTE24, farnesyl-prelamin A accumulates in the nucleus and exerts toxicity, causing a variety of disease phenotypes. By ∼4 months of age, both male and female Zmpste24-/- mice manifest a near-complete loss of adipose tissue, but it has never been clear whether this phenotype is a direct consequence of farnesyl-prelamin A toxicity in adipocytes. To address this question, we generated a conditional knockout Zmpste24 allele and used it to create adipocyte-specific Zmpste24-knockout mice. To boost farnesyl-prelamin A levels, we bred in the "prelamin A-only" Lmna allele. Gene expression, immunoblotting, and immunohistochemistry experiments revealed that adipose tissue in these mice had decreased Zmpste24 expression along with strikingly increased accumulation of prelamin A. In male mice, Zmpste24 deficiency in adipocytes was accompanied by modest changes in adipose stores (an 11% decrease in body weight, a 23% decrease in body fat mass, and significantly smaller gonadal and inguinal white adipose depots). No changes in adipose stores were detected in female mice, likely because prelamin A expression in adipose tissue is lower in female mice. Zmpste24 deficiency in adipocytes did not alter the number of macrophages in adipose tissue, nor did it alter plasma levels of glucose, triglycerides, or fatty acids. We conclude that ZMPSTE24 deficiency in adipocytes, and the accompanying accumulation of farnesyl-prelamin A, reduces adipose tissue stores, but only modestly and only in male mice.

Published
2020

3. Mutating a conserved cysteine in GPIHBP1 reduces amounts of GPIHBP1 in capillaries and abolishes LPL binding

Author

Allan, Christopher M, Jung, Cris J, Larsson, Mikael, Heizer, Patrick J, Tu, Yiping, Sandoval, Norma P, Dang, Tiffany Ly P, Jung, Rachel S, Beigneux, Anne P, de Jong, Pieter J, Fong, Loren G, and Young, Stephen G

Subjects
Biochemistry and Cell Biology, Biomedical and Clinical Sciences, Biological Sciences, Generic health relevance, Animals, CHO Cells, Conserved Sequence, Cricetinae, Cricetulus, Cysteine, Female, Humans, Lipoprotein Lipase, Mice, Mutation, Protein Binding, RNA, Messenger, Receptors, Lipoprotein, Triglycerides, chylomicrons, endothelial cells, lipids/chemistry, lipolysis and fatty acid metabolism, triglycerides, glycosylphosphatidylinositol-anchored HDL binding protein 1, lipoprotein lipase, Medical Biochemistry and Metabolomics, Biochemistry & Molecular Biology, Biochemistry and cell biology, Medical biochemistry and metabolomics
Abstract

Mutation of conserved cysteines in proteins of the Ly6 family cause human disease-chylomicronemia in the case of glycosylphosphatidylinositol-anchored HDL binding protein 1 (GPIHBP1) and paroxysmal nocturnal hemoglobinuria in the case of CD59. A mutation in a conserved cysteine in CD59 prevented the protein from reaching the surface of blood cells. In contrast, mutation of conserved cysteines in human GPIHBP1 had little effect on GPIHBP1 trafficking to the surface of cultured CHO cells. The latter findings were somewhat surprising and raised questions about whether CHO cell studies accurately model the fate of mutant GPIHBP1 proteins in vivo. To explore this concern, we created mice harboring a GPIHBP1 cysteine mutation (p.C63Y). The p.C63Y mutation abolished the ability of mouse GPIHBP1 to bind LPL, resulting in severe chylomicronemia. The mutant GPIHBP1 was detectable by immunohistochemistry on the surface of endothelial cells, but the level of expression was ∼70% lower than in WT mice. The mutant GPIHBP1 protein in mouse tissues was predominantly monomeric. We conclude that mutation of a conserved cysteine in GPIHBP1 abolishes the ability of GPIHBP1 to bind LPL, resulting in mislocalization of LPL and severe chylomicronemia. The mutation reduced but did not eliminate GPIHBP1 on the surface of endothelial cells in vivo.

Published
2017

4. Efficient gene targeting in mouse zygotes mediated by CRISPR/Cas9-protein

Author

Jung, Chris J, Zhang, Junli, Trenchard, Elizabeth, Lloyd, Kent C, West, David B, Rosen, Barry, and de Jong, Pieter J

Subjects
Biochemistry and Cell Biology, Biological Sciences, Stem Cell Research, Genetics, Stem Cell Research - Embryonic - Non-Human, Biotechnology, 1.1 Normal biological development and functioning, Generic health relevance, Alleles, Animals, CRISPR-Cas Systems, DNA End-Joining Repair, Exons, Gene Targeting, Homologous Recombination, Mice, RNA, Guide, CRISPR-Cas Systems, RNA, Messenger, Zygote, CRISPR, Transgenic mouse model, Gene targeting, Technology, Plant Biology & Botany, Biological sciences
Abstract

The CRISPR/Cas9 system has rapidly advanced targeted genome editing technologies. However, its efficiency in targeting with constructs in mouse zygotes via homology directed repair (HDR) remains low. Here, we systematically explored optimal parameters for targeting constructs in mouse zygotes via HDR using mouse embryonic stem cells as a model system. We characterized several parameters, including single guide RNA cleavage activity and the length and symmetry of homology arms in the construct, and we compared the targeting efficiency between Cas9, Cas9nickase, and dCas9-FokI. We then applied the optimized conditions to zygotes, delivering Cas9 as either mRNA or protein. We found that Cas9 nucleo-protein complex promotes highly efficient, multiplexed targeting of circular constructs containing reporter genes and floxed exons. This approach allows for a one-step zygote injection procedure targeting multiple genes to generate conditional alleles via homologous recombination, and simultaneous knockout of corresponding genes in non-targeted alleles via non-homologous end joining.

Published
2017

5. Gain of Toxicity from ALS/FTD-Linked Repeat Expansions in C9ORF72 Is Alleviated by Antisense Oligonucleotides Targeting GGGGCC-Containing RNAs

Author

Jiang, Jie, Zhu, Qiang, Gendron, Tania F, Saberi, Shahram, McAlonis-Downes, Melissa, Seelman, Amanda, Stauffer, Jennifer E, Jafar-nejad, Paymaan, Drenner, Kevin, Schulte, Derek, Chun, Seung, Sun, Shuying, Ling, Shuo-Chien, Myers, Brian, Engelhardt, Jeffery, Katz, Melanie, Baughn, Michael, Platoshyn, Oleksandr, Marsala, Martin, Watt, Andy, Heyser, Charles J, Ard, M Colin, De Muynck, Louis, Daughrity, Lillian M, Swing, Deborah A, Tessarollo, Lino, Jung, Chris J, Delpoux, Arnaud, Utzschneider, Daniel T, Hedrick, Stephen M, de Jong, Pieter J, Edbauer, Dieter, Van Damme, Philip, Petrucelli, Leonard, Shaw, Christopher E, Bennett, C Frank, Da Cruz, Sandrine, Ravits, John, Rigo, Frank, Cleveland, Don W, and Lagier-Tourenne, Clotilde

Subjects
Biological Psychology, Biomedical and Clinical Sciences, Neurosciences, Psychology, Brain Disorders, Genetics, Dementia, Neurodegenerative, Acquired Cognitive Impairment, Behavioral and Social Science, ALS, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Frontotemporal Dementia (FTD), Rare Diseases, Aetiology, 2.1 Biological and endogenous factors, Neurological, Amyotrophic Lateral Sclerosis, Animals, C9orf72 Protein, DNA Repeat Expansion, Frontotemporal Dementia, Guanine Nucleotide Exchange Factors, Mice, Transgenic, Neurons, Oligonucleotides, Antisense, RNA, Cognitive Sciences, Neurology & Neurosurgery, Biological psychology
Abstract

Hexanucleotide expansions in C9ORF72 are the most frequent genetic cause of amyotrophic lateral sclerosis and frontotemporal dementia. Disease mechanisms were evaluated in mice expressing C9ORF72 RNAs with up to 450 GGGGCC repeats or with one or both C9orf72 alleles inactivated. Chronic 50% reduction of C9ORF72 did not provoke disease, while its absence produced splenomegaly, enlarged lymph nodes, and mild social interaction deficits, but not motor dysfunction. Hexanucleotide expansions caused age-, repeat-length-, and expression-level-dependent accumulation of RNA foci and dipeptide-repeat proteins synthesized by AUG-independent translation, accompanied by loss of hippocampal neurons, increased anxiety, and impaired cognitive function. Single-dose injection of antisense oligonucleotides (ASOs) that target repeat-containing RNAs but preserve levels of mRNAs encoding C9ORF72 produced sustained reductions in RNA foci and dipeptide-repeat proteins, and ameliorated behavioral deficits. These efforts identify gain of toxicity as a central disease mechanism caused by repeat-expanded C9ORF72 and establish the feasibility of ASO-mediated therapy.

Published
2016

6. Transcriptome Analysis of Targeted Mouse Mutations Reveals the Topography of Local Changes in Gene Expression.

Author

West, David B, Engelhard, Eric K, Adkisson, Michael, Nava, AJ, Kirov, Julia V, Cipollone, Andreanna, Willis, Brandon, Rapp, Jared, de Jong, Pieter J, and Lloyd, Kent C

Subjects
Animals, Mice, Inbred C57BL, Gene Expression Profiling, Gene Targeting, Gene Expression Regulation, Down-Regulation, Up-Regulation, Gene Deletion, Homozygote, Mutation, Gene Library, Genome, Mice, Inbred C57BL, Genetics, Developmental Biology
Abstract

The unintended consequences of gene targeting in mouse models have not been thoroughly studied and a more systematic analysis is needed to understand the frequency and characteristics of off-target effects. Using RNA-seq, we evaluated targeted and neighboring gene expression in tissues from 44 homozygous mutants compared with C57BL/6N control mice. Two allele types were evaluated: 15 targeted trap mutations (TRAP); and 29 deletion alleles (DEL), usually a deletion between the translational start and the 3' UTR. Both targeting strategies insert a bacterial beta-galactosidase reporter (LacZ) and a neomycin resistance selection cassette. Evaluating transcription of genes in +/- 500 kb of flanking DNA around the targeted gene, we found up-regulated genes more frequently around DEL compared with TRAP alleles, however the frequency of alleles with local down-regulated genes flanking DEL and TRAP targets was similar. Down-regulated genes around both DEL and TRAP targets were found at a higher frequency than expected from a genome-wide survey. However, only around DEL targets were up-regulated genes found with a significantly higher frequency compared with genome-wide sampling. Transcriptome analysis confirms targeting in 97% of DEL alleles, but in only 47% of TRAP alleles probably due to non-functional splice variants, and some splicing around the gene trap. Local effects on gene expression are likely due to a number of factors including compensatory regulation, loss or disruption of intragenic regulatory elements, the exogenous promoter in the neo selection cassette, removal of insulating DNA in the DEL mutants, and local silencing due to disruption of normal chromatin organization or presence of exogenous DNA. An understanding of local position effects is important for understanding and interpreting any phenotype attributed to targeted gene mutations, or to spontaneous indels.

Published
2016

7. A lacZ reporter gene expression atlas for 313 adult KOMP mutant mouse lines

Author

West, David B, Pasumarthi, Ravi K, Baridon, Brian, Djan, Esi, Trainor, Amanda, Griffey, Stephen M, Engelhard, Eric K, Rapp, Jared, Li, Bowen, de Jong, Pieter J, and Lloyd, KC Kent

Subjects
Biological Sciences, Genetics, Biotechnology, Animals, Atlases as Topic, Female, Gene Expression, Gene Expression Regulation, Genes, Reporter, Lac Operon, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Promoter Regions, Genetic, Staining and Labeling, Structure-Activity Relationship, Medical and Health Sciences, Bioinformatics
Abstract

Expression of the bacterial beta-galactosidase reporter gene (lacZ) in the vector used for the Knockout Mouse Project (KOMP) is driven by the endogenous promoter of the target gene. In tissues from KOMP mice, histochemical staining for LacZ enzyme activity can be used to determine gene expression patterns. With this technique, we have produced a comprehensive resource of gene expression using both whole mount (WM) and frozen section (FS) LacZ staining in 313 unique KOMP mutant mouse lines. Of these, ∼ 80% of mutants showed specific staining in one or more tissues, while ∼ 20% showed no specific staining, ∼ 13% had staining in only one tissue, and ∼ 25% had staining in >6 tissues. The highest frequency of specific staining occurred in the brain (∼ 50%), male gonads (42%), and kidney (39%). The WM method was useful for rapidly identifying whole organ and some substructure staining, while the FS method often revealed substructure and cellular staining specificity. Both staining methods had >90% repeatability in biological replicates. Nonspecific LacZ staining occurs in some tissues due to the presence of bacteria or endogenous enzyme activity. However, this can be effectively distinguished from reporter gene activity by the combination of the WM and FS methods. After careful annotation, LacZ staining patterns in a high percentage of mutants revealed a unique structure-function not previously reported for many of these genes. The validation of methods for LacZ staining, annotation, and expression analysis reported here provides unique insights into the function of genes for which little is currently known.

Published
2015

8. Sphingosine-1-phosphate lyase downregulation promotes colon carcinogenesis through STAT3-activated microRNAs

Author

Degagné, Emilie, Pandurangan, Ashok, Bandhuvula, Padmavathi, Kumar, Ashok, Eltanawy, Abeer, Zhang, Meng, Yoshinaga, Yuko, Nefedov, Mikhail, de Jong, Pieter J, Fong, Loren G, Young, Stephen G, Bittman, Robert, Ahmedi, Yasmin, and Saba, Julie D

Subjects
Biological Sciences, Biomedical and Clinical Sciences, Health Sciences, Cancer, Autoimmune Disease, Inflammatory Bowel Disease, Genetics, Colo-Rectal Cancer, Digestive Diseases, Prevention, 2.1 Biological and endogenous factors, Aldehyde-Lyases, Animals, Anion Transport Proteins, Biopsy, Cell Transformation, Neoplastic, Colonic Neoplasms, Down-Regulation, Gene Deletion, Gene Expression Regulation, Enzymologic, Gene Expression Regulation, Neoplastic, Humans, Inflammatory Bowel Diseases, Lysophospholipids, Mice, Mice, Transgenic, MicroRNAs, Neoplasm Proteins, Neoplasms, Experimental, RNA, Neoplasm, STAT3 Transcription Factor, Signal Transduction, Sphingosine, Medical and Health Sciences, Immunology, Biological sciences, Biomedical and clinical sciences, Health sciences
Abstract

Growing evidence supports a link between inflammation and cancer; however, mediators of the transition between inflammation and carcinogenesis remain incompletely understood. Sphingosine-1-phosphate (S1P) lyase (SPL) irreversibly degrades the bioactive sphingolipid S1P and is highly expressed in enterocytes but downregulated in colon cancer. Here, we investigated the role of SPL in colitis-associated cancer (CAC). We generated mice with intestinal epithelium-specific Sgpl1 deletion and chemically induced colitis and tumor formation in these animals. Compared with control animals, mice lacking intestinal SPL exhibited greater disease activity, colon shortening, cytokine levels, S1P accumulation, tumors, STAT3 activation, STAT3-activated microRNAs (miRNAs), and suppression of miR-targeted anti-oncogene products. This phenotype was attenuated by STAT3 inhibition. In fibroblasts, silencing SPL promoted tumorigenic transformation through a pathway involving extracellular transport of S1P through S1P transporter spinster homolog 2 (SPNS2), S1P receptor activation, JAK2/STAT3-dependent miR-181b-1 induction, and silencing of miR-181b-1 target cylindromatosis (CYLD). Colon biopsies from patients with inflammatory bowel disease revealed enhanced S1P and STAT3 signaling. In mice with chemical-induced CAC, oral administration of plant-type sphingolipids called sphingadienes increased colonic SPL levels and reduced S1P levels, STAT3 signaling, cytokine levels, and tumorigenesis, indicating that SPL prevents transformation and carcinogenesis. Together, our results suggest that dietary sphingolipids can augment or prevent colon cancer, depending upon whether they are metabolized to S1P or promote S1P metabolism through the actions of SPL.

Published
2014

9. Reciprocal knock-in mice to investigate the functional redundancy of lamin B1 and lamin B2

Author

Lee, John M, Tu, Yiping, Tatar, Angelica, Wu, Daniel, Nobumori, Chika, Jung, Hea-Jin, Yoshinaga, Yuko, Coffinier, Catherine, de Jong, Pieter J, Fong, Loren G, and Young, Stephen G

Subjects
Biochemistry and Cell Biology, Biological Sciences, Pediatric, Genetics, Brain Disorders, Neurological, Amino Acid Sequence, Animals, Cerebral Cortex, Gene Knock-In Techniques, Lamin Type B, Mice, Mice, Inbred C57BL, Mice, Knockout, Neural Tube Defects, Neurogenesis, Nuclear Lamina, Sequence Analysis, DNA, Medical and Health Sciences, Developmental Biology, Biochemistry and cell biology
Abstract

Lamins B1 and B2 (B-type lamins) have very similar sequences and are expressed ubiquitously. In addition, both Lmnb1- and Lmnb2-deficient mice die soon after birth with neuronal layering abnormalities in the cerebral cortex, a consequence of defective neuronal migration. The similarities in amino acid sequences, expression patterns, and knockout phenotypes raise the question of whether the two proteins have redundant functions. To investigate this topic, we generated "reciprocal knock-in mice"-mice that make lamin B2 from the Lmnb1 locus (Lmnb1(B2/B2)) and mice that make lamin B1 from the Lmnb2 locus (Lmnb2(B1/B1)). Lmnb1(B2/B2) mice produced increased amounts of lamin B2 but no lamin B1; they died soon after birth with neuronal layering abnormalities in the cerebral cortex. However, the defects in Lmnb1(B2/B2) mice were less severe than those in Lmnb1-knockout mice, indicating that increased amounts of lamin B2 partially ameliorate the abnormalities associated with lamin B1 deficiency. Similarly, increased amounts of lamin B1 in Lmnb2(B1/B1) mice did not prevent the neurodevelopmental defects elicited by lamin B2 deficiency. We conclude that lamins B1 and B2 have unique roles in the developing brain and that increased production of one B-type lamin does not fully complement loss of the other.

Published
2014

10. Sequencing and Assembly of the 22-Gb Loblolly Pine Genome

Author

Zimin, Aleksey, Stevens, Kristian A, Crepeau, Marc W, Holtz-Morris, Ann, Koriabine, Maxim, Marçais, Guillaume, Puiu, Daniela, Roberts, Michael, Wegrzyn, Jill L, de Jong, Pieter J, Neale, David B, Salzberg, Steven L, Yorke, James A, and Langley, Charles H

Subjects
Genetics, Human Genome, Biotechnology, Generic health relevance, Genome, Plant, Genomics, Haploidy, Ovule, Pinus taeda, Sequence Analysis, DNA, Transcriptome, placeholder, denovo assembly, loblolly pine, (see cocoa genome), Pinus taeda L., conifer, de novo assembly, fosmid, genome, Developmental Biology
Abstract

Conifers are the predominant gymnosperm. The size and complexity of their genomes has presented formidable technical challenges for whole-genome shotgun sequencing and assembly. We employed novel strategies that allowed us to determine the loblolly pine (Pinus taeda) reference genome sequence, the largest genome assembled to date. Most of the sequence data were derived from whole-genome shotgun sequencing of a single megagametophyte, the haploid tissue of a single pine seed. Although that constrained the quantity of available DNA, the resulting haploid sequence data were well-suited for assembly. The haploid sequence was augmented with multiple linking long-fragment mate pair libraries from the parental diploid DNA. For the longest fragments, we used novel fosmid DiTag libraries. Sequences from the linking libraries that did not match the megagametophyte were identified and removed. Assembly of the sequence data were aided by condensing the enormous number of paired-end reads into a much smaller set of longer "super-reads," rendering subsequent assembly with an overlap-based assembly algorithm computationally feasible. To further improve the contiguity and biological utility of the genome sequence, additional scaffolding methods utilizing independent genome and transcriptome assemblies were implemented. The combination of these strategies resulted in a draft genome sequence of 20.15 billion bases, with an N50 scaffold size of 66.9 kbp.

Published
2014

11. Unique Features of the Loblolly Pine (Pinus taeda L.) Megagenome Revealed Through Sequence Annotation

Author

Wegrzyn, Jill L, Liechty, John D, Stevens, Kristian A, Wu, Le-Shin, Loopstra, Carol A, Vasquez-Gross, Hans A, Dougherty, William M, Lin, Brian Y, Zieve, Jacob J, Martínez-García, Pedro J, Holt, Carson, Yandell, Mark, Zimin, Aleksey V, Yorke, James A, Crepeau, Marc W, Puiu, Daniela, Salzberg, Steven L, de Jong, Pieter J, Mockaitis, Keithanne, Main, Doreen, Langley, Charles H, and Neale, David B

Subjects
Biological Sciences, Genetics, DNA, Plant, Evolution, Molecular, Genes, Plant, Genome, Plant, Molecular Sequence Annotation, Multigene Family, Phylogeny, Pinus taeda, Sequence Alignment, introns, gene family, repeats, retrotransposons, conifer, Developmental Biology, Biochemistry and cell biology
Abstract

The largest genus in the conifer family Pinaceae is Pinus, with over 100 species. The size and complexity of their genomes (∼20-40 Gb, 2n = 24) have delayed the arrival of a well-annotated reference sequence. In this study, we present the annotation of the first whole-genome shotgun assembly of loblolly pine (Pinus taeda L.), which comprises 20.1 Gb of sequence. The MAKER-P annotation pipeline combined evidence-based alignments and ab initio predictions to generate 50,172 gene models, of which 15,653 are classified as high confidence. Clustering these gene models with 13 other plant species resulted in 20,646 gene families, of which 1554 are predicted to be unique to conifers. Among the conifer gene families, 159 are composed exclusively of loblolly pine members. The gene models for loblolly pine have the highest median and mean intron lengths of 24 fully sequenced plant genomes. Conifer genomes are full of repetitive DNA, with the most significant contributions from long-terminal-repeat retrotransposons. In depth analysis of the tandem and interspersed repetitive content yielded a combined estimate of 82%.

Published
2014

12. Author Correction: Comparative and demographic analysis of orang-utan genomes

Author

Locke, Devin P., Hillier, LaDeana W., Warren, Wesley C., Worley, Kim C., Nazareth, Lynne V., Muzny, Donna M., Yang, Shiaw-Pyng, Wang, Zhengyuan, Chinwalla, Asif T., Minx, Pat, Mitreva, Makedonka, Cook, Lisa, Delehaunty, Kim D., Fronick, Catrina, Schmidt, Heather, Fulton, Lucinda A., Fulton, Robert S., Nelson, Joanne O., Magrini, Vincent, Pohl, Craig, Graves, Tina A., Markovic, Chris, Cree, Andy, Dinh, Huyen H., Hume, Jennifer, Kovar, Christie L., Fowler, Gerald R., Lunter, Gerton, Meader, Stephen, Heger, Andreas, Ponting, Chris P., Marques-Bonet, Tomas, Alkan, Can, Chen, Lin, Cheng, Ze, Kidd, Jeffrey M., Eichler, Evan E., White, Simon, Searle, Stephen, Vilella, Albert J., Chen, Yuan, Flicek, Paul, Ma, Jian, Raney, Brian, Suh, Bernard, Burhans, Richard, Herrero, Javier, Haussler, David, Faria, Rui, Fernando, Olga, Darré, Fleur, Farré, Domènec, Gazave, Elodie, Oliva, Meritxell, Navarro, Arcadi, Roberto, Roberta, Capozzi, Oronzo, Archidiacono, Nicoletta, Della Valle, Giuliano, Purgato, Stefania, Rocchi, Mariano, Konkel, Miriam K., Walker, Jerilyn A., Ullmer, Brygg, Batzer, Mark A., Smit, Arian F. A., Hubley, Robert, Casola, Claudio, Schrider, Daniel R., Hahn, Matthew W., Quesada, Victor, Puente, Xose S., Ordoñez, Gonzalo R., López-Otín, Carlos, Vinar, Tomas, Brejova, Brona, Ratan, Aakrosh, Harris, Robert S., Miller, Webb, Kosiol, Carolin, Lawson, Heather A., Taliwal, Vikas, Martins, André L., Siepel, Adam, RoyChoudhury, Arindam, Ma, Xin, Degenhardt, Jeremiah, Bustamante, Carlos D., Gutenkunst, Ryan N., Mailund, Thomas, Dutheil, Julien Y., Hobolth, Asger, Schierup, Mikkel H., Ryder, Oliver A., Yoshinaga, Yuko, de Jong, Pieter J., Weinstock, George M., Rogers, Jeffrey, Mardis, Elaine R., Gibbs, Richard A., and Wilson, Richard K.

Published
2022
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13. microRNA-1 regulates sarcomere formation and suppresses smooth muscle gene expression in the mammalian heart.

Author

Heidersbach, Amy, Saxby, Chris, Carver-Moore, Karen, Huang, Yu, Ang, Yen-Sin, de Jong, Pieter J, Ivey, Kathryn N, and Srivastava, Deepak

Subjects
Sarcomeres, Muscle, Smooth, Myocardium, Animals, Mice, Knockout, Mice, MicroRNAs, Gene Expression, Phosphorylation, Myocardin, Telokin, cardiac, microRNA-1, sarcomere, smooth muscle gene expression, Muscle, Smooth, Knockout, Biochemistry and Cell Biology
Abstract

microRNA-1 (miR-1) is an evolutionarily conserved, striated muscle-enriched miRNA. Most mammalian genomes contain two copies of miR-1, and in mice, deletion of a single locus, miR-1-2, causes incompletely penetrant lethality and subtle cardiac defects. Here, we report that deletion of miR-1-1 resulted in a phenotype similar to that of the miR-1-2 mutant. Compound miR-1 knockout mice died uniformly before weaning due to severe cardiac dysfunction. miR-1-null cardiomyocytes had abnormal sarcomere organization and decreased phosphorylation of the regulatory myosin light chain-2 (MLC2), a critical cytoskeletal regulator. The smooth muscle-restricted inhibitor of MLC2 phosphorylation, Telokin, was ectopically expressed in the myocardium, along with other smooth muscle genes. miR-1 repressed Telokin expression through direct targeting and by repressing its transcriptional regulator, Myocardin. Our results reveal that miR-1 is required for postnatal cardiac function and reinforces the striated muscle phenotype by regulating both transcriptional and effector nodes of the smooth muscle gene expression network. DOI: http://dx.doi.org/10.7554/eLife.01323.001.

Published
2013

14. The mammalian gene function resource: the International Knockout Mouse Consortium.

Author

Bradley, Allan, Anastassiadis, Konstantinos, Ayadi, Abdelkader, Battey, James F, Bell, Cindy, Birling, Marie-Christine, Bottomley, Joanna, Brown, Steve D, Bürger, Antje, Bult, Carol J, Bushell, Wendy, Collins, Francis S, Desaintes, Christian, Doe, Brendan, Economides, Aris, Eppig, Janan T, Finnell, Richard H, Fletcher, Colin, Fray, Martin, Frendewey, David, Friedel, Roland H, Grosveld, Frank G, Hansen, Jens, Hérault, Yann, Hicks, Geoffrey, Hörlein, Andreas, Houghton, Richard, Hrabé de Angelis, Martin, Huylebroeck, Danny, Iyer, Vivek, de Jong, Pieter J, Kadin, James A, Kaloff, Cornelia, Kennedy, Karen, Koutsourakis, Manousos, Lloyd, KC Kent, Marschall, Susan, Mason, Jeremy, McKerlie, Colin, McLeod, Michael P, von Melchner, Harald, Moore, Mark, Mujica, Alejandro O, Nagy, Andras, Nefedov, Mikhail, Nutter, Lauryl M, Pavlovic, Guillaume, Peterson, Jane L, Pollock, Jonathan, Ramirez-Solis, Ramiro, Rancourt, Derrick E, Raspa, Marcello, Remacle, Jacques E, Ringwald, Martin, Rosen, Barry, Rosenthal, Nadia, Rossant, Janet, Ruiz Noppinger, Patricia, Ryder, Ed, Schick, Joel Zupicich, Schnütgen, Frank, Schofield, Paul, Seisenberger, Claudia, Selloum, Mohammed, Simpson, Elizabeth M, Skarnes, William C, Smedley, Damian, Stanford, William L, Stewart, A Francis, Stone, Kevin, Swan, Kate, Tadepally, Hamsa, Teboul, Lydia, Tocchini-Valentini, Glauco P, Valenzuela, David, West, Anthony P, Yamamura, Ken-ichi, Yoshinaga, Yuko, and Wurst, Wolfgang

Subjects
Animals, Mice, Knockout, Mice, Internationality, Internet, Knockout, Genetics, Genetics & Heredity
Abstract

In 2007, the International Knockout Mouse Consortium (IKMC) made the ambitious promise to generate mutations in virtually every protein-coding gene of the mouse genome in a concerted worldwide action. Now, 5 years later, the IKMC members have developed high-throughput gene trapping and, in particular, gene-targeting pipelines and generated more than 17,400 mutant murine embryonic stem (ES) cell clones and more than 1,700 mutant mouse strains, most of them conditional. A common IKMC web portal (www.knockoutmouse.org) has been established, allowing easy access to this unparalleled biological resource. The IKMC materials considerably enhance functional gene annotation of the mammalian genome and will have a major impact on future biomedical research.

Published
2012

15. Deficiencies in lamin B1 and lamin B2 cause neurodevelopmental defects and distinct nuclear shape abnormalities in neurons

Author

Coffinier, Catherine, Jung, Hea-Jin, Nobumori, Chika, Chang, Sandy, Tu, Yiping, Barnes, Richard H, Yoshinaga, Yuko, de Jong, Pieter J, Vergnes, Laurent, Reue, Karen, Fong, Loren G, and Young, Stephen G

Subjects
Biochemistry and Cell Biology, Biological Sciences, Genetics, Neurosciences, Neurological, Animals, Brain, Lamin Type B, Mice, Mice, Knockout, Neurons, Nuclear Lamina, Prosencephalon, Medical and Health Sciences, Developmental Biology, Biochemistry and cell biology
Abstract

Neuronal migration is essential for the development of the mammalian brain. Here, we document severe defects in neuronal migration and reduced numbers of neurons in lamin B1-deficient mice. Lamin B1 deficiency resulted in striking abnormalities in the nuclear shape of cortical neurons; many neurons contained a solitary nuclear bleb and exhibited an asymmetric distribution of lamin B2. In contrast, lamin B2 deficiency led to increased numbers of neurons with elongated nuclei. We used conditional alleles for Lmnb1 and Lmnb2 to create forebrain-specific knockout mice. The forebrain-specific Lmnb1- and Lmnb2-knockout models had a small forebrain with disorganized layering of neurons and nuclear shape abnormalities, similar to abnormalities identified in the conventional knockout mice. A more severe phenotype, complete atrophy of the cortex, was observed in forebrain-specific Lmnb1/Lmnb2 double-knockout mice. This study demonstrates that both lamin B1 and lamin B2 are essential for brain development, with lamin B1 being required for the integrity of the nuclear lamina, and lamin B2 being important for resistance to nuclear elongation in neurons.

Published
2011

16. Patterns of Genetic Variation Within and Between Gibbon Species

Author

Kim, Sung K, Carbone, Lucia, Becquet, Celine, Mootnick, Alan R, Li, David Jiang, de Jong, Pieter J, and Wall, Jeffrey D

Subjects
Biological Sciences, Ecology, Evolutionary Biology, Genetics, Life on Land, Animals, Cell Line, Gene Flow, Genetic Linkage, Genetic Variation, Hylobates, Mutation, Phenotype, Phylogeny, population history, chromosomal rearrangements, genetic diversity, gibbon, population genetics, Biochemistry and Cell Biology, Biochemistry and cell biology, Evolutionary biology
Abstract

Gibbons are small, arboreal, highly endangered apes that are understudied compared with other hominoids. At present, there are four recognized genera and approximately 17 species, all likely to have diverged from each other within the last 5-6 My. Although the gibbon phylogeny has been investigated using various approaches (i.e., vocalization, morphology, mitochondrial DNA, karyotype, etc.), the precise taxonomic relationships are still highly debated. Here, we present the first survey of nuclear sequence variation within and between gibbon species with the goal of estimating basic population genetic parameters. We gathered ~60 kb of sequence data from a panel of 19 gibbons representing nine species and all four genera. We observe high levels of nucleotide diversity within species, indicative of large historical population sizes. In addition, we find low levels of genetic differentiation between species within a genus comparable to what has been estimated for human populations. This is likely due to ongoing or episodic gene flow between species, and we estimate a migration rate between Nomascus leucogenys and N. gabriellae of roughly one migrant every two generations. Together, our findings suggest that gibbons have had a complex demographic history involving hybridization or mixing between diverged populations.

Published
2011

18. Evolutionary breakpoints in the gibbon suggest association between cytosine methylation and karyotype evolution.

Author

Carbone, Lucia, Harris, R Alan, Vessere, Gery M, Mootnick, Alan R, Humphray, Sean, Rogers, Jane, Kim, Sung K, Wall, Jeffrey D, Martin, David, Jurka, Jerzy, Milosavljevic, Aleksandar, and de Jong, Pieter J

Subjects
Animals, Humans, Hylobates, Cytosine, Chromosome Mapping, Karyotyping, Evolution, Molecular, Species Specificity, DNA Methylation, Epigenesis, Genetic, Gene Rearrangement, Alu Elements, Synteny, Genome, Human, Models, Genetic, DNA Breaks, Epigenesis, Genetic, Evolution, Molecular, Genome, Human, Models, Genetics, Developmental Biology
Abstract

Gibbon species have accumulated an unusually high number of chromosomal changes since diverging from the common hominoid ancestor 15-18 million years ago. The cause of this increased rate of chromosomal rearrangements is not known, nor is it known if genome architecture has a role. To address this question, we analyzed sequences spanning 57 breaks of synteny between northern white-cheeked gibbons (Nomascus l. leucogenys) and humans. We find that the breakpoint regions are enriched in segmental duplications and repeats, with Alu elements being the most abundant. Alus located near the gibbon breakpoints (

Published
2009

19. Construction and Analysis of a Human-Chimpanzee Comparative Clone Map

Author

Fujiyama, Asao, Watanabe, Hidemi, Toyoda, Atsushi, Taylor, Todd D., Itoh, Takehiko, Tsai, Shih-Feng, Park, Hong-Seog, Yaspo, Marie-Laure, Lehrach, Hans, Chen, Zhu, Fu, Gang, Saitou, Naruya, Osoegawa, Kazutoyo, de Jong, Pieter J., Suto, Yumiko, Hattori, Masahira, and Sakaki, Yoshiyuki

Published
2002

21. A BAC-Based Physical Map of the Major Autosomes of Drosophila melanogaster

Author

Hoskins, Roger A., Nelson, Catherine R., Berman, Benjamin P., Laverty, Todd R., George, Reed A., Ciesiolka, Lisa, Naeemuddin, Mohammed, Arenson, Andrew D., Durbin, James, David, Robert G., Tabor, Paul E., Bailey, Michael R., DeShazo, Denise R., Catanese, Joseph, Mammoser, Aaron, Osoegawa, Kazutoyo, de Jong, Pieter J., Celniker, Susan E., Gibbs, Richard A., Rubin, Gerald M., and Scherer, Steven E.

Published
2000

22. The Genomic Sequence of the Accidental Pathogen Legionella pneumophila

Author

Chien, Minchen, Morozova, Irina, Shi, Shundi, Sheng, Huitao, Chen, Jing, Gomez, Shawn M., Asamani, Gifty, Hill, Kendra, Nuara, John, Feder, Marc, Rineer, Justin, Greenberg, Joseph J., Steshenko, Valeria, Park, Samantha H., Zhao, Baohui, Teplitskaya, Elita, Edwards, John R., Pampou, Sergey, Georghiou, Anthi, Iannuccilli, William, Ulz, Michael E., Kim, Dae H., Geringer-Sameth, Alex, Goldsberry, Curtis, Morozov, Pavel, Fischer, Stuart G., Segal, Gil, Qu, Xiaoyan, Rzhetsky, Andrey, Zhang, Peisen, Cayanis, Eftihia, De Jong, Pieter J., Ju, Jingyue, Kalachikov, Sergey, Shuman, Howard A., and Russo, James J.

Published
2004

26. A Resource for the Conditional Ablation of microRNAs in the Mouse

Author

Park, Chong Yon, Jeker, Lukas T., Carver-Moore, Karen, Oh, Alyssia, Liu, Huey Jiin, Cameron, Rachel, Richards, Hunter, Li, Zhongmei, Adler, David, Yoshinaga, Yuko, Martinez, Maria, Nefadov, Michael, Abbas, Abul K., Weiss, Art, Lanier, Lewis L., de Jong, Pieter J., Bluestone, Jeffrey A., Srivastava, Deepak, and McManus, Michael T.

Published
2012
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27. Massively Parallel Sequencing Identifies the Gene Megf8 with ENU-Induced Mutation Causing Heterotaxy

Author

Zhang, Zhen, Alpert, Deanne, Francis, Richard, Chatterjee, Bishwanath, Yu, Qing, Tansey, Terry, Sabol, Steven L., Cui, Cheng, Bai, Yongli, Koriabine, Maxim, Yoshinaga, Yuko, Cheng, Jan-Fang, Chen, Feng, Martin, Joel, Schackwitz, Wendy, Gunn, Teresa M., Kramer, Kenneth L., De Jong, Pieter J., Pennacchio, Len A., Lo, Cecilia W., and Nirenberg, Marshall

Published
2009
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29. Draft Genome Sequence of the Sexually Transmitted Pathogen Trichomonas vaginalis

Author

Carlton, Jane M., Hirt, Robert P., Silva, Joana C., Delcher, Arthur L., Schatz, Michael, Zhao, Qi, Wortman, Jennifer R., Bidwell, Shelby L., Alsmark, U. Cecilia M., Besteiro, Sébastien, Sicheritz-Ponten, Thomas, Noel, Christophe J., Dacks, Joel B., Foster, Peter G., Simillion, Cedric, Van de Peer, Yves, Miranda-Saavedra, Diego, Barton, Geoffrey J., Westrop, Gareth D., Müller, Sylke, Dessi, Daniele, Fiori, Pier Luigi, Ren, Qinghu, Paulsen, Ian, Zhang, Hanbang, Bastida-Corcuera, Felix D., Simoes-Barbosa, Augusto, Brown, Mark T., Hayes, Richard D., Mukherjee, Mandira, Okumura, Cheryl Y., Schneider, Rachel, Smith, Alias J., Vanacova, Stepanka, Villalvazo, Maria, Haas, Brian J., Pertea, Mihaela, Feldblyum, Tamara V., Utterback, Terry R., Shu, Chung-Li, Osoegawa, Kazutoyo, de Jong, Pieter J., Hrdy, Ivan, Horvathova, Lenka, Zubacova, Zuzana, Dolezal, Pavel, Malik, Shehre-Banoo, Logsdon, John M., Henze, Katrin, Gupta, Arti, Wang, Ching C., Dunne, Rebecca L., Upcroft, Jacqueline A., Upcroft, Peter, White, Owen, Salzberg, Steven L., Tang, Petrus, Chiu, Cheng-Hsun, Lee, Ying-Shiung, Embley, T. Martin, Coombs, Graham H., Mottram, Jeremy C., Tachezy, Jan, Fraser-Liggett, Claire M., and Johnson, Patricia J.

Published
2007
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30. Gibbon genome and the fast karyotype evolution of small apes

Author

Carbone, Lucia, Alan Harris, R., Gnerre, Sante, Veeramah, Krishna R., Lorente-Galdos, Belen, Huddleston, John, Meyer, Thomas J., Herrero, Javier, Roos, Christian, Aken, Bronwen, Anaclerio, Fabio, Archidiacono, Nicoletta, Baker, Carl, Barrell, Daniel, Batzer, Mark A., Beal, Kathryn, Blancher, Antoine, Bohrson, Craig L., Brameier, Markus, Campbell, Michael S., Capozzi, Oronzo, Casola, Claudio, Chiatante, Giorgia, Cree, Andrew, Damert, Annette, de Jong, Pieter J., Dumas, Laura, Fernandez-Callejo, Marcos, Flicek, Paul, Fuchs, Nina V., Gut, Ivo, Gut, Marta, Hahn, Matthew W., Hernandez-Rodriguez, Jessica, Hillier, LaDeana W., Hubley, Robert, Ianc, Bianca, Izsvák, Zsuzsanna, Jablonski, Nina G., Johnstone, Laurel M., Karimpour-Fard, Anis, Konkel, Miriam K., Kostka, Dennis, Lazar, Nathan H., Lee, Sandra L., Lewis, Lora R., Liu, Yue, Locke, Devin P., Mallick, Swapan, Mendez, Fernando L., Muffato, Matthieu, Nazareth, Lynne V., Nevonen, Kimberly A., O’Bleness, Majesta, Ochis, Cornelia, Odom, Duncan T., Pollard, Katherine S., Quilez, Javier, Reich, David, Rocchi, Mariano, Schumann, Gerald G., Searle, Stephen, Sikela, James M., Skollar, Gabriella, Smit, Arian, Sonmez, Kemal, Hallers, Boudewijn ten, Terhune, Elizabeth, Thomas, Gregg W. C., Ullmer, Brygg, Ventura, Mario, Walker, Jerilyn A., Wall, Jeffrey D., Walter, Lutz, Ward, Michelle C., Wheelan, Sarah J., Whelan, Christopher W., White, Simon, Wilhelm, Larry J., Woerner, August E., Yandell, Mark, Zhu, Baoli, Hammer, Michael F., Marques-Bonet, Tomas, Eichler, Evan E., Fulton, Lucinda, Fronick, Catrina, Muzny, Donna M., Warren, Wesley C., Worley, Kim C., Rogers, Jeffrey, Wilson, Richard K., and Gibbs, Richard A.

Published
2014
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31. Genome-wide end-sequenced BAC resources for the NOD/MrkTac☆ and NOD/ShiLtJ☆☆ mouse genomes

Author

Steward, Charles A., Humphray, Sean, Plumb, Bob, Jones, Matthew C., Quail, Michael A., Rice, Stephen, Cox, Tony, Davies, Rob, Bonfield, James, Keane, Thomas M., Nefedov, Michael, de Jong, Pieter J., Lyons, Paul, Wicker, Linda, Todd, John, Hayashizaki, Yoshihide, Gulban, Omid, Danska, Jayne, Harrow, Jen, Hubbard, Tim, Rogers, Jane, and Adams, David J.

Published
2010
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37. Comparative and demographic analysis of orang-utan genomes

Author

Locke, Devin P., Hillier, LaDeana W., Warren, Wesley C., Worley, Kim C., Nazareth, Lynne V., Muzny, Donna M., Yang, Shiaw-Pyng, Wang, Zhengyuan, Chinwalla, Asif T., Minx, Pat, Mitreva, Makedonka, Cook, Lisa, Delehaunty, Kim D., Fronick, Catrina, Schmidt, Heather, Fulton, Lucinda A., Fulton, Robert S., Nelson, Joanne O., Magrini, Vincent, Pohl, Craig, Graves, Tina A., Markovic, Chris, Cree, Andy, Dinh, Huyen H., Hume, Jennifer, Kovar, Christie L., Fowler, Gerald R., Lunter, Gerton, Meader, Stephen, Heger, Andreas, Ponting, Chris P., Marques-Bonet, Tomas, Alkan, Can, Chen, Lin, Cheng, Ze, Kidd, Jeffrey M., Eichler, Evan E., White, Simon, Searle, Stephen, Vilella, Albert J., Chen, Yuan, Flicek, Paul, Ma, Jian, Raney, Brian, Suh, Bernard, Burhans, Richard, Herrero, Javier, Haussler, David, Faria, Rui, Fernando, Olga, Darré, Fleur, Farré, Domènec, Gazave, Elodie, Oliva, Meritxell, Navarro, Arcadi, Roberto, Roberta, Capozzi, Oronzo, Archidiacono, Nicoletta, Valle, Giuliano Della, Purgato, Stefania, Rocchi, Mariano, Konkel, Miriam K., Walker, Jerilyn A., Ullmer, Brygg, Batzer, Mark A., Smit, Arian F. A., Hubley, Robert, Casola, Claudio, Schrider, Daniel R., Hahn, Matthew W., Quesada, Victor, Puente, Xose S., Ordoñez, Gonzalo R., López-Otín, Carlos, Vinar, Tomas, Brejova, Brona, Ratan, Aakrosh, Harris, Robert S., Miller, Webb, Kosiol, Carolin, Lawson, Heather A., Taliwal, Vikas, Martins, André L., Siepel, Adam, RoyChoudhury, Arindam, Ma, Xin, Degenhardt, Jeremiah, Bustamante, Carlos D., Gutenkunst, Ryan N., Mailund, Thomas, Dutheil, Julien Y., Hobolth, Asger, Schierup, Mikkel H., Ryder, Oliver A., Yoshinaga, Yuko, de Jong, Pieter J., Weinstock, George M., Rogers, Jeffrey, Mardis, Elaine R., Gibbs, Richard A., and Wilson, Richard K.

Published
2011
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39. Variation analysis and gene annotation of eight MHC haplotypes: The MHC Haplotype Project

Author

Horton, Roger, Gibson, Richard, Coggill, Penny, Miretti, Marcos, Allcock, Richard J., Almeida, Jeff, Forbes, Simon, Gilbert, James G. R., Halls, Karen, Harrow, Jennifer L., Hart, Elizabeth, Howe, Kevin, Jackson, David K., Palmer, Sophie, Roberts, Anne N., Sims, Sarah, Stewart, C. Andrew, Traherne, James A., Trevanion, Steve, Wilming, Laurens, Rogers, Jane, de Jong, Pieter J., Elliott, John F., Sawcer, Stephen, Todd, John A., Trowsdale, John, and Beck, Stephan

Published
2008
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40. The amphioxus genome and the evolution of the chordate karyotype

Author

Putnam, Nicholas H., Butts, Thomas, Ferrier, David E.K., Furlong, Rebecca F., Hellsten, Uffe, Kawashima, Takeshi, Robinson-Rechavi, Marc, Shoguchi, Eiichi, Terry, Astrid, Yu, Jr-Kai, Benito-Gutierrez, Elia, Dubchak, Inna, Garcia-Fernandez, Jordi, Gibson-Brown, Jeremy J., Grigoriev, Igor V., Horton, Amy C., de Jong, Pieter J., Jurka, Jerzy, Kapitonov, Vladimir V., Kohara, Yuji, Kuroki, Yoko, Lindquist, Erika, Lucas, Susan, Osoegawa, Kazutoyo, Pennacchio, Len A., Salamov, Asaf A., Satou, Yutaka, Sauka-Spengler, Tatjana, Schmutz, Jeremy, Shin-I, Tadasu, Toyoda, Atsushi, Bronner-Fraser, Marianne, Fujiyama, Asao, Holland, Linda Z., Holland, Peter W.H., Satoh, Nori, and Rokhsar, Daniel S.

Subjects
Genomes -- Identification and classification -- Genetic aspects, Genetic variation -- Evaluation -- Genetic aspects, Karyotypes -- Identification and classification -- Genetic aspects, Environmental issues, Science and technology, Zoology and wildlife conservation, Identification and classification, Evaluation, Genetic aspects, Natural history
Abstract

Lancelets ('amphioxus') are the modern survivors of an ancient chordate lineage, with a fossil record dating back to the Cambrian period. Here we describe the structure and gene content of [...]

Published
2008

42. DNA sequence of human chromosome 17 and analysis of rearrangement in the human lineage

Author

Zody, Michael C., Garber, Manuel, Adams, David J., Sharpe, Ted, Harrow, Jennifer, Lupski, James R., Nicholson, Christine, Searle, Steven M., Wilming, Laurens, Young, Sarah K., Abouelleil, Amr, Allen, Nicole R., Bi, Weimin, Bloom, Toby, Borowsky, Mark L., Bugalter, Boris E., Butler, Jonathan, Chang, Jean L., Chen, Chao-Kung, Cook, April, Corum, Benjamin, Cuomo, Christina A., de Jong, Pieter J., DeCaprio, David, Dewar, Ken, FitzGerald, Michael, Gilbert, James, Gibson, Richard, Gnerre, Sante, Goldstein, Steven, Grafham, Darren V., Grocock, Russell, Hafez, Nabil, Hagopian, Daniel S., Hart, Elizabeth, Norman, Catherine Hosage, Humphray, Sean, Jaffe, David B., Jones, Matt, Kamal, Michael, Khodiyar, Varsha K., LaButti, Kurt, Laird, Gavin, Lehoczky, Jessica, Liu, Xiaohong, Lokyitsang, Tashi, Loveland, Jane, Lui, Annie, Macdonald, Pendexter, Major, John E., Matthews, Lucy, Mauceli, Evan, McCarroll, Steven A., Mihalev, Atanas H., Mudge, Jonathan, Nguyen, Cindy, Nicol, Robert, O'Leary, Sinéad B., Osoegawa, Kazutoyo, Schwartz, David C., Shaw-Smith, Charles, Stankiewicz, Pawel, Steward, Charles, Swarbreck, David, Venkataraman, Vijay, Whittaker, Charles A., Yang, Xiaoping, Zimmer, Andrew R., Bradley, Allan, Hubbard, Tim, Birren, Bruce W., Rogers, Jane, Lander, Eric S., and Nusbaum, Chad

Published
2006
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43. Downregulation of Death-Associated Protein Kinase 1 (DAPK1) in Chronic Lymphocytic Leukemia

Author

Raval, Aparna, Tanner, Stephan M., Byrd, John C., Angerman, Elizabeth B., Perko, James D., Chen, Shih-Shih, Hackanson, Björn, Grever, Michael R., Lucas, David M., Matkovic, Jennifer J., Lin, Thomas S., Kipps, Thomas J., Murray, Fiona, Weisenburger, Dennis, Sanger, Warren, Lynch, Jane, Watson, Patrice, Jansen, Mary, Yoshinaga, Yuko, Rosenquist, Richard, de Jong, Pieter J., Coggill, Penny, Beck, Stephan, Lynch, Henry, de la Chapelle, Albert, and Plass, Christoph

Published
2007
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44. Identification and analysis of functional elements in 1% of the human genome by the ENCODE pilot project

Author

Birney, Ewan, Stamatoyannopoulos, John A., Dutta, Anindya, Guigo, Roderic, Gingeras, Thomas R., Margulies, Elliott H., Weng, Zhiping, Snyder, Michael, Dermitzakis, Emmanouil T., Thurman, Robert E., Kuehn, Michael S., Taylor, Christopher M., Neph, Shane, Koch, Christoph M., Asthana, Saurabh, Malhotra, Ankit, Adzhubei, Ivan, Greenbaum, Jason A., Andrews, Robert M., Flicek, Paul, Boyle, Patrick J., Cao, Hua, Carter, Nigel P., Clelland, Gayle K., Davis, Sean, Day, Nathan, Dhami, Pawandeep, Dillon, Shane C., Dorschner, Michael O., Fiegler, Heike, Giresi, Paul G., Goldy, Jeff, Hawrylycz, Michael, Haydock, Andrew, Humbert, Richard, James, Keith D., Johnson, Brett E., Johnson, Ericka M., Frum, Tristan T., Rosenzweig, Elizabeth R., Karnani, Neerja, Lee, Kirsten, Lefebvre, Gregory C., Navas, Patrick A., Neri, Fidencio, Parker, Stephen C. J., Sabo, Peter J., Sandstrom, Richard, Shafer, Anthony, Vetrie, David, Weaver, Molly, Wilcox, Sarah, Yu1, Man, Collins, Francis S., Dekker, Job, Lieb, Jason D., Tullius, Thomas D., Crawford, Gregory E., Sunyaev, Shamil, Noble, William S., Dunham, Ian, Denoeud, France, Reymond, Alexandre, Kapranov, Philipp, Rozowsky, Joel, Zheng, Deyou, Castelo, Robert, Frankish, Adam, Harrow, Jennifer, Ghosh, Srinka, Sandelin, Albin, Hofacker, Ivo L., Baertsch, Robert, Keefe, Damian, Dike, Sujit, Cheng, Jill, Hirsch, Heather A., Sekinger, Edward A., Lagarde, Julien, Abril, Josep F., Shahab, Atif, Flamm, Christoph, Fried, Claudia, Hackermuller, Jorg, Hertel, Jana, Lindemeyer, Manja, Missal, Kristin, Tanzer, Andrea, Washietl, Stefan, Korbel, Jan, Emanuelsson, Olof, Pedersen, Jakob S., Holroyd, Nancy, Taylor, Ruth, Swarbreck, David, Matthews, Nicholas, Dickson, Mark C., Thomas, Daryl J., Weirauch, Matthew T., Gilbert, James, Drenkow, Jorg, Bell, Ian, Zhao, XiaoDong, Srinivasan, K.G., Sung, Wing-Kin, Ooi, Hong Sain, Chiu, Kuo Ping, Foissac, Sylvain, Alioto, Tyler, Brent, Michael, Pachter, Lior, Tress, Michael L., Valencia, Alfonso, Choo, Siew Woh, Choo, Chiou Yu, Ucla, Catherine, Manzano, Caroline, Wyss, Carine, Cheung, Evelyn, Clark, Taane G., Brown, James B., Ganesh, Madhavan, Patel, Sandeep, Tammana, Hari, Chrast, Jacqueline, Henrichsen, Charlotte N., Kai, Chikatoshi, Kawai, Jun, Nagalakshmi, Ugrappa, Wu, Jiaqian, Lian, Zheng, Lian, Jin, Newburger, Peter, Zhang, Xueqing, Bickel, Peter, Mattick, John S., Carninci, Piero, Hayashizaki, Yoshihide, Weissman, Sherman, Hubbard, Tim, Myers, Richard M., Rogers, Jane, Stadler, Peter F., Lowe, Todd M., Wei, Chia-Lin, Ruan, Yijun, Struhl, Kevin, Gerstein, Mark, Antonarakis, Stylianos E., Fu, Yutao, Green, Eric D., Karaoz, Ulaş, Siepel, Adam, Taylor, James, Liefer, Laura A., Wetterstrand, Kris A., Good, Peter J., Feingold, Elise A., Guyer, Mark S., Cooper, Gregory M., Asimenos, George, Dewey, Colin N., Hou, Minmei, Nikolaev, Sergey, Montoya-Burgos, Juan I., Loytynoja, Ari, Whelan, Simon, Pardi, Fabio, Massingham, Tim, Huang, Haiyan, Zhang, Nancy R., Holmes, Ian, Mullikin, James C., Ureta-Vidal, Abel, Paten, Benedict, Seringhaus, Michael, Church, Deanna, Rosenbloom, Kate, Kent, W. James, Stone, Eric A., Batzoglou, Serafim, Goldman, Nick, Hardison, Ross C., Haussler, David, Miller, Webb, Sidow, Arend, Trinklein, Nathan D., Zhang, Zhengdong D., Barrera, Leah, Stuart, Rhona, King, David C., Ameur, Adam, Enroth, Stefan, Bieda, Mark C., Kim, Jonghwan, Bhinge, Akshay A., Jiang, Nan, Liu, Jun, Yao, Fei, Vega, Vinsensius B., Lee, Charlie W.H., Ng, Patrick, Yang, Annie, Moqtaderi, Zarmik, Zhu, Zhou, Xu, Xiaoqin, Squazzo, Sharon, Oberley, Matthew J., Inman, David, Singer, Michael A., Richmond, Todd A., Munn, Kyle J., Rada-Iglesias, Alvaro, Wallerman, Ola, Komorowski, Jan, Fowler, Joanna C., Couttet, Phillippe, Bruce, Alexander W., Dovey, Oliver M., Ellis, Peter D., Langford, Cordelia F., Nix, David A., Euskirchen, Ghia, Hartman, Stephen, Urban, Alexander E., Kraus, Peter, Van Calcar, Sara, Heintzman, Nate, Hoon Kim, Tae, Wang, Kun, Qu, Chunxu, Hon, Gary, Luna, Rosa, Glass, Christopher K., Rosenfeld, M. Geoff, Aldred, Shelley Force, Cooper, Sara J., Halees, Anason, Lin, Jane M., Shulha, Hennady P., Zhang, Xiaoling, Xu, Mousheng, Haidar, Jaafar N. S., Yu, Yong, Birney*, Ewan, Iyer, Vishwanath R., Green, Roland D., Wadelius, Claes, Farnham, Peggy J., Ren, Bing, Harte, Rachel A., Hinrichs, Angie S., Trumbower, Heather, Clawson, Hiram, Hillman-Jackson, Jennifer, Zweig, Ann S., Smith, Kayla, Thakkapallayil, Archana, Barber, Galt, Kuhn, Robert M., Karolchik, Donna, Armengol, Lluis, Bird, Christine P., de Bakker, Paul I. W., Kern, Andrew D., Lopez-Bigas, Nuria, Martin, Joel D., Stranger, Barbara E., Woodroffe, Abigail, Davydov, Eugene, Dimas, Antigone, Eyras, Eduardo, Hallgrimsdottir, Ingileif B., Huppert, Julian, Zody, Michael C., Abecasis, Goncalo R., Estivill, Xavier, Bouffard, Gerard G., Guan, Xiaobin, Hansen, Nancy F., Idol, Jacquelyn R., Maduro, Valerie V.B., Maskeri, Baishali, McDowell, Jennifer C., Park, Morgan, Thomas, Pamela J., Young, Alice C., Blakesley, Robert W., Baylor College of Medicine, Human Genome Sequencing Center, Muzny, Donna M., Sodergren, Erica, Wheeler, David A., Worley, Kim C., Jiang, Huaiyang, Weinstock, George M., Gibbs, Richard A., Graves, Tina, Fulton, Robert, Mardis, Elaine R., Wilson, Richard K., Clamp, Michele, Cuff, James, Gnerre, Sante, Jaffe, David B., Chang, Jean L., Lindblad-Toh, Kerstin, Lander, Eric S., Koriabine, Maxim, Nefedov, Mikhail, Osoegawa, Kazutoyo, Yoshinaga, Yuko, Zhu, Baoli, and de Jong, Pieter J.

Subjects
Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

Author(s): The ENCODE Project Consortium; Analysis Coordination; Ewan Birney (corresponding author) [1]; John A. Stamatoyannopoulos (corresponding author) [2]; Anindya Dutta (corresponding author) [3]; Roderic Guigó (corresponding author) [4, 5]; Thomas [...]

Published
2007
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46. A physical map of the chicken genome

Author

Wallis, John W., Aerts, Jan, Groenen, Martien A. M., Crooijmans, Richard P. M. A., Layman, Dan, Graves, Tina A., Scheer, Debra E., Kremitzki, Colin, Fedele, Mary J., Mudd, Nancy K., Cardenas, Marco, Higginbotham, Jamey, Carter, Jason, McGrane, Rebecca, Gaige, Tony, Mead, Kelly, Walker, Jason, Albracht, Derek, Davito, Jonathan, Yang, Shiaw-Pyng, Leong, Shin, Chinwalla, Asif, Sekhon, Mandeep, Wylie, Kristine, Dodgson, Jerry, Romanov, Michael N., Cheng, Hans, de Jong, Pieter J., Osoegawa, Kazutoyo, Nefedov, Mikhail, Zhang, Hongbin, McPherson, John D., Krzywinski, Martin, Schein, Jacquie, Hillier, LaDeana, Mardis, Elaine R., Wilson, Richard K., and Warren, Wesley C.

Published
2004
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47. The DNA sequence of the human X chromosome

Author

Ross, Mark T., Grafham, Darren V., Coffey, Alison J., Scherer, Steven, McLay, Kirsten, Muzny, Donna, Platzer, Matthias, Howell, Gareth R., Burrows, Christine, Bird, Christine P., Frankish, Adam, Lovell, Frances L., Howe, Kevin L., Ashurst, Jennifer L., Fulton, Robert S., Sudbrak, Ralf, Wen, Gaiping, Jones, Matthew C., Hurles, Matthew E., Andrews, T. Daniel, Scott, Carol E., Searle, Stephen, Ramser, Juliane, Whittaker, Adam, Deadman, Rebecca, Carter, Nigel P., Hunt, Sarah E., Chen, Rui, Cree, Andrew, Gunaratne, Preethi, Havlak, Paul, Hodgson, Anne, Metzker, Michael L., Richards, Stephen, Scott, Graham, Steffen, David, Sodergren, Erica, Wheeler, David A., Worley, Kim C., Ainscough, Rachael, Ambrose, Kerrie D., Ansari-Lari, M. Ali, Aradhya, Swaroop, Ashwell, Robert I. S., Babbage, Anne K., Bagguley, Claire L., Ballabio, Andrea, Banerjee, Ruby, Barker, Gary E., Barlow, Karen F., Barrett, Ian P., Bates, Karen N., Beare, David M., Beasley, Helen, Beasley, Oliver, Beck, Alfred, Bethel, Graeme, Blechschmidt, Karin, Brady, Nicola, Bray-Allen, Sarah, Bridgeman, Anne M., Brown, Andrew J., Brown, Mary J., Bonnin, David, Bruford, Elspeth A., Buhay, Christian, Burch, Paula, Burford, Deborah, Burgess, Joanne, Burrill, Wayne, Burton, John, Bye, Jackie M., Carder, Carol, Carrel, Laura, Chako, Joseph, Chapman, Joanne C., Chavez, Dean, Chen, Ellson, Chen, Guan, Chen, Yuan, Chen, Zhijian, Chinault, Craig, Ciccodicola, Alfredo, Clark, Sue Y., Clarke, Graham, Clee, Chris M., Clegg, Sheila, Clerc-Blankenburg, Kerstin, Clifford, Karen, Cobley, Vicky, Cole, Charlotte G., Conquer, Jen S., Corby, Nicole, Connor, Richard E., David, Robert, Davies, Joy, Davis, Clay, Davis, John, Delgado, Oliver, DeShazo, Denise, Dhami, Pawandeep, Ding, Yan, Dinh, Huyen, Dodsworth, Steve, Draper, Heather, Dugan-Rocha, Shannon, Dunham, Andrew, Dunn, Matthew, Durbin, K. James, Dutta, Ireena, Eades, Tamsin, Ellwood, Matthew, Emery-Cohen, Alexandra, Errington, Helen, Evans, Kathryn L., Faulkner, Louisa, Francis, Fiona, Frankland, John, Fraser, Audrey E., Galgoczy, Petra, Gilbert, James, Gill, Rachel, Glockner, Gernot, Gregory, Simon G., Gribble, Susan, Griffiths, Coline, Grocock, Russell, Gu, Yanghong, Gwilliam, Rhian, Hamilton, Cerissa, Hart, Elizabeth A., Hawes, Alicia, Heath, Paul D., Heitmann, Katja, Hennig, Steffen, Hernandez, Judith, Hinzmann, Bernd, Ho, Sarah, Hoffs, Michael, Howden, Phillip J., Huckle, Elizabeth J., Hume, Jennifer, Hunt, Paul J., Hunt, Adrienne R., Isherwood, Judith, Jacob, Leni, Johnson, David, Jones, Sally, de Jong, Pieter J., Joseph, Shirin S., Keenan, Stephen, Kelly, Susan, Kershaw, Joanne K., Khan, Ziad, Kioschis, Petra, Klages, Sven, Knights, Andrew J., Kosiura, Anna, Kovar-Smith, Christie, Laird, Gavin K., Langford, Cordelia, Lawlor, Stephanie, Leversha, Margaret, Lewis, Lora, Liu, Wen, Lloyd, Christine, Lloyd, David M., Loulseged, Hermela, Loveland, Jane E., Lovell, Jamieson D., Lozado, Ryan, Lu, Jing, Lyne, Rachael, Ma, Jie, Maheshwari, Manjula, Matthews, Lucy H., McDowall, Jennifer, McLaren, Stuart, McMurray, Amanda, Meidl, Patrick, Meitinger, Thomas, Milne, Sarah, Miner, George, Mistry, Shailesh L., Morgan, Margaret, Morris, Sidney, Muller, Ines, Mullikin, James C., Nguyen, Ngoc, Nordsiek, Gabriele, Nyakatura, Gerald, O'Dell, Christopher N., Okwuonu, Geoffery, Palmer, Sophie, Pandian, Richard, Parker, David, Parrish, Julia, Pasternak, Shiran, Patel, Dina, Pearce, Alex V., Pearson, Danita M., Pelan, Sarah E., Perez, Lesette, Porter, Keith M., Ramsey, Yvonne, Reichwald, Kathrin, Rhodes, Susan, Ridler, Kerry A., Schlessinger, David, Schueler, Mary G., Sehra, Harminder K., Shaw-Smith, Charles, Shen, Hua, Sheridan, Elizabeth M., Shownkeen, Ratna, Skuce, Carl D., Smith, Michelle L., Sotheran, Elizabeth C., Steingruber, Helen E., Steward, Charles A., Storey, Roy, Swann, R. Mark, Swarbreck, David, Tabor, Paul E., Taudien, Stefan, Taylor, Tineace, Teague, Brian, Thomas, Karen, Thorpe, Andrea, Timms, Kirsten, Tracey, Alan, Trevanion, Steve, Tromans, Anthony C., d'Urso, Michele, Verduzco, Daniel, Villasana, Donna, Waldron, Lenee, Wall, Melanie, Wang, Qiaoyan, Warren, James, Warry, Georgina L., Wei, Xuehong, West, Anthony, Whitehead, Siobhan L., Whiteley, Mathew N., Wilkinson, Jane E., Willey, David L., Williams, Gabrielle, Williams, Leanne, Williamson, Angela, Williamson, Helen, Wilming, Laurens, Woodmansey, Rebecca L., Wray, Paul W., Yen, Jennifer, Zhang, Jingkun, Zhou, Jianling, Zoghbi, Huda, Zorilla, Sara, Buck, David, Reinhardt, Richard, Poustka, Annemarie, Rosenthal, Andre, Lehrach, Hans, Meindl, Alfons, Minx, Patrick J., Hillier, LaDeana W., Willard, Huntington F., Wilson, Richard K., Waterston, Robert H., Rice, Catherine M., Vaudin, Mark, Coulson, Alan, Nelson, David L., Weinstock, George, Sulston, John E., Durbin, Richard, Hubbard, Tim, Gibbs, Richard A., Beck, Stephan, Rogers, Jane, and Bentley, David R.

Subjects
Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

Author(s): Mark T. Ross (corresponding author) [1]; Darren V. Grafham [1]; Alison J. Coffey [1]; Steven Scherer [2]; Kirsten McLay [1]; Donna Muzny [2]; Matthias Platzer [3]; Gareth R. Howell [...]

Published
2005
Full Text
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48. The zebrafish reference genome sequence and its relationship to the human genome

Author

Howe, Kerstin, Clark, Matthew D., Torroja, Carlos F., Torrance, James, Berthelot, Camille, Muffato, Matthieu, Collins, John E., Humphray, Sean, McLaren, Karen, Matthews, Lucy, McLaren, Stuart, Sealy, Ian, Caccamo, Mario, Churcher, Carol, Scott, Carol, Barrett, Jeffrey C., Koch, Romke, Rauch, Gerd-Jörg, White, Simon, Chow, William, Kilian, Britt, Quintais, Leonor T., Guerra-Assunção, José A., Zhou, Yi, Gu, Yong, Yen, Jennifer, Vogel, Jan-Hinnerk, Eyre, Tina, Redmond, Seth, Banerjee, Ruby, Chi, Jianxiang, Fu, Beiyuan, Langley, Elizabeth, Maguire, Sean F., Laird, Gavin K., Lloyd, David, Kenyon, Emma, Donaldson, Sarah, Sehra, Harminder, Almeida-King, Jeff, Loveland, Jane, Trevanion, Stephen, Jones, Matt, Quail, Mike, Willey, Dave, Hunt, Adrienne, Burton, John, Sims, Sarah, McLay, Kirsten, Plumb, Bob, Davis, Joy, Clee, Chris, Oliver, Karen, Clark, Richard, Riddle, Clare, Eliott, David, Threadgold, Glen, Harden, Glenn, Ware, Darren, Mortimer, Beverly, Kerry, Giselle, Heath, Paul, Phillimore, Benjamin, Tracey, Alan, Corby, Nicole, Dunn, Matthew, Johnson, Christopher, Wood, Jonathan, Clark, Susan, Pelan, Sarah, Griffiths, Guy, Smith, Michelle, Glithero, Rebecca, Howden, Philip, Barker, Nicholas, Stevens, Christopher, Harley, Joanna, Holt, Karen, Panagiotidis, Georgios, Lovell, Jamieson, Beasley, Helen, Henderson, Carl, Gordon, Daria, Auger, Katherine, Wright, Deborah, Collins, Joanna, Raisen, Claire, Dyer, Lauren, Leung, Kenric, Robertson, Lauren, Ambridge, Kirsty, Leongamornlert, Daniel, McGuire, Sarah, Gilderthorp, Ruth, Griffiths, Coline, Manthravadi, Deepa, Nichol, Sarah, Barker, Gary, Whitehead, Siobhan, Kay, Michael, Brown, Jacqueline, Murnane, Clare, Gray, Emma, Humphries, Matthew, Sycamore, Neil, Barker, Darren, Saunders, David, Wallis, Justene, Babbage, Anne, Hammond, Sian, Mashreghi-Mohammadi, Maryam, Barr, Lucy, Martin, Sancha, Wray, Paul, Ellington, Andrew, Matthews, Nicholas, Ellwood, Matthew, Woodmansey, Rebecca, Clark, Graham, Cooper, James, Tromans, Anthony, Grafham, Darren, Skuce, Carl, Pandian, Richard, Andrews, Robert, Harrison, Elliot, Kimberley, Andrew, Garnett, Jane, Fosker, Nigel, Hall, Rebekah, Garner, Patrick, Kelly, Daniel, Bird, Christine, Palmer, Sophie, Gehring, Ines, Berger, Andrea, Dooley, Christopher M., Ersan-Ürün, Zübeyde, Eser, Cigdem, Geiger, Horst, Geisler, Maria, Karotki, Lena, Kirn, Anette, Konantz, Judith, Konantz, Martina, Oberländer, Martina, Rudolph-Geiger, Silke, Teucke, Mathias, Osoegawa, Kazutoyo, Zhu, Baoli, Rapp, Amanda, Widaa, Sara, Langford, Cordelia, Yang, Fengtang, Carter, Nigel P., Harrow, Jennifer, Ning, Zemin, Herrero, Javier, Searle, Steve M. J., Enright, Anton, Geisler, Robert, Plasterk, Ronald H. A., Lee, Charles, Westerfield, Monte, de Jong, Pieter J., Zon, Leonard I., Postlethwait, John H., Nüsslein-Volhard, Christiane, Hubbard, Tim J. P., Crollius, Hugues Roest, Rogers, Jane, and Stemple, Derek L.

Published
2013
Full Text
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