Transcriptomic profiling of mature embryo from an elite super-hybrid rice LYP9 and its parental lines

BMC Plant Biology， 2008, 8:114，Xiaomeng Ge，Jun Yu

Transcriptomic profiling of mature embryo from an elite super-hybrid rice LYP9 and its parental lines

Xiaomeng Ge* 1,2 , Weihua Chen* 1 , Shuhui Song1,2 , Weiwei Wang1,2 , Songnian Hu1  and Jun Yu1

1CAS Key Laboratory of Genome Sciences and Information, Beijing Institute of Genomics, Chinese Academy of Sciences, Beijing, 100029, PR China

2Graduate University of Chinese Academy of Sciences, Beijing, 100049, PR China

Background

The mature embryo of rice (Oryza sativa, L.) is a synchronized and integrated tissue mass laying the foundation at molecular level for its growth, development, and differentiation toward a developing and ultimately a mature plant. We carried out an EST (expressed-sequence-tags)-based transcriptomic study, aiming at gaining molecular insights into embryonic development of a rice hybrid triad–an elite hybrid rice LYP9 and its parental lines (93-11 and PA64s)–and possible relatedness to heterosis.

Results

We generated 27,566 high-quality ESTs from cDNA libraries made from mature rice embryos. We classified these ESTs into 7,557 unigenes (2,511 contigs and 5,046 singletons) and 7,250 (95.9%) of them were annotated. We noticed that the high-abundance genes in mature rice embryos belong to two major functional categories, stress-tolerance and preparation-for-development, and we also identified 191 differentially-expressed genes (General Chi-squared test, P-value <= 0.05) between LYP9 and its parental lines, representing typical expression patterns including over-dominance, high- and low-parent dominance, additivity, and under-dominance. In LYP9, the majority of embryo-associated genes were found not only abundantly and specifically enriched but also significantly up-regulated.

Conclusion

Our results suggested that massively strengthening tissue-(or stage-) characteristic functions may contribute to heterosis rather than a few simple mechanistic explanations at the individual gene level. In addition, the large collection of rice embryonic ESTs provides significant amount of data for future comparative analyses on plant development, especially for the important crops of the grass family.

How Complex Movements Of Enzymes Make Fat

How Complex Movements Of Enzymes Make Fat
ScienceDaily (Feb. 20, 2009) — A groundbreaking study has revealed in great detail how enzymes in the cell cooperate to make fat. These enzymes are integrated into a single molecular complex known as fatty acid synthase. This complex is regarded as a potential target for developing new anti-obesity and anti-cancer drugs.

Dr. Stuart Smith, at Children's Hospital Oakland Research Institute, collaborated with Drs. Edward Brignole and Francisco Asturias from The Scripps Research Institute in La Jolla, Calif. in a study published in the February 2009 edition of Nature Structural and Molecular Biology and featured on the cover of the journal.

"Fatty Acid Synthase is a remarkably complex structure. It contains all of the components needed to convert carbohydrates into fat," Dr. Smith explained. "We have suspected for some time that the enzyme complex is extremely flexible, which makes it difficult to analyze using X-ray crystallography. Last year the X-ray structure of the complex was solved by a group in Switzerland, but this structure provided only a snapshot of the complex in one of its many poses. We were able to use state-of-the-art electron microscopy to obtain images of the complex in many of its different conformations and assemble these images into a movie that displays the full range of motion of the components of the complex." The results reveal how enzymes that appear distantly located in the X-ray structure are able to make the contacts with each other needed for catalysis. The extraordinary swinging, swiveling and rolling motions of fatty acid synthase are represented on the cover of the journal in the form of a flamenco dancer.

Some pharmaceutical companies are focusing on inhibitors of fatty acid synthase because they are known to block the conversion of carbohydrates into fat and suppress appetite as well as slow the growth of cancer cells. Structural information garnered from X-ray and electron microscope images may aid in the design of more effective inhibitors that could be used therapeutically.

 

Cellular prion protein mediates impairment of synaptic plasticity by amyloid-β oligomers

Nature 457, 1128-1132 (26 February 2009) | doi:10.1038/nature07761

Cellular prion protein mediates impairment of synaptic plasticity by amyloid-β oligomers

Juha Laurén1, David A. Gimbel1, Haakon B. Nygaard1, John W. Gilbert1 & Stephen M. Strittmatter1

Cellular Neuroscience, Neurodegeneration and Repair Program, Yale University School of Medicine, New Haven, Connecticut 06536, USA

Correspondence to: Stephen M. Strittmatter1 Correspondence and requests for materials should be addressed to S.M.S.

A pathological hallmark of Alzheimer's disease is an accumulation of insoluble plaque containing the amyloid-β peptide of 40�42 amino acid residues1. Prefibrillar, soluble oligomers of amyloid-β have been recognized to be early and key intermediates in Alzheimer's-disease-related synaptic dysfunction2, 3, 4, 5, 6, 7, 8, 9. At nanomolar concentrations, soluble amyloid-β oligomers block hippocampal long-term potentiation7, cause dendritic spine retraction from pyramidal cells5, 8 and impair rodent spatial memory2. Soluble amyloid- oligomers have been prepared from chemical syntheses, transfected cell culture supernatants, transgenic mouse brain and human Alzheimer's disease brain2, 4, 7, 9. Together, these data imply a high-affinity cell-surface receptor for soluble amyloid- oligomers on neurons―one that is central to the pathophysiological process in Alzheimer's disease. Here we identify the cellular prion protein (PrP^c) as an amyloid-β-oligomer receptor by expression cloning. Amyloid- oligomers bind with nanomolar affinity to PrP^c, but the interaction does not require the infectious PrP^Sc conformation. Synaptic responsiveness in hippocampal slices from young adult PrP null mice is normal, but the amyloid-β oligomer blockade of long-term potentiation is absent. Anti-PrP antibodies prevent amyloid-β-oligomer binding to PrP^c and rescue synaptic plasticity in hippocampal slices from oligomeric amyloid-β. Thus, PrP^c is a mediator of amyloid-β-oligomer-induced synaptic dysfunction, and PrP^c-specific pharmaceuticals may have therapeutic potential for Alzheimer's disease.

Antibody Recognition of a Highly Conserved Influenza Virus Epitope

Damian C. Ekiert 1, Gira Bhabha 1, Marc-André Elsliger 1, Robert H. E. Friesen 2, Mandy Jongeneelen 2, Mark Throsby 2, Jaap Goudsmit 2, Ian A. Wilson 3*

1 Department of Molecular Biology, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA.
2 Crucell Holland BV, Archimedesweg 4-6, 2301 CA Leiden, The Netherlands.
3 Department of Molecular Biology, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA.; The Skaggs Institute for Chemical Biology, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA.

Influenza virus presents a significant and persistent threat to public health worldwide, and current vaccines provide immunity to viral isolates similar to the vaccine strain. High-affinity antibodies against a conserved epitope could provide immunity to the diverse influenza subtypes and protection against future pandemic viruses. Co-crystal structures were determined at 2.2 and 2.7 ? resolutions for broadly neutralizing human antibody CR6261 Fab in complexes with the major surface antigen (hemagglutinin, HA) from viruses responsible for the 1918 H1N1 influenza pandemic and a recent lethal case of H5N1 avian influenza. In contrast to other structurally characterized influenza antibodies, CR6261 recognizes a highly conserved helical region in the membrane-proximal stem of HA1/HA2. The antibody neutralizes the virus by blocking conformational rearrangements associated with membrane fusion. The CR6261 epitope identified here should accelerate the design and implementation of improved vaccines that can elicit CR6261-like antibodies, as well as antibody-based therapies for the treatment of influenza.

The oral jaws of Pseudotropheus elongatus.

The oral jaws of Pseudotropheus elongatus.

The jaws of vertebrates, their origins, and their associated dentitions have long been a topic of interest among both paleontologists and evolutionary developmental biologists. The modern diversity of Lake Malawi cichlids has been used here to offer a new perspective on the relationships between teeth on two sets of functional jawsâ€"oral and pharyngealâ€"and the origins of the vertebrate dentition in the throat of jawless fishes some 500 million years ago (see Fraser et al., e1000031).

The Atonal Proneural Transcription Factor Links Differentiation and Tumor Formation in Drosophila

Drosophila

【Abstract】

The acquisition of terminal cell fate and onset of differentiation are instructed by cell type–specific master control genes. Loss of differentiation is frequently observed during cancer progression, but the underlying causes and mechanisms remain poorly understood. We tested the hypothesis that master regulators of differentiation may be key regulators of tumor formation. Using loss- and gain-of-function analyses in Drosophila, we describe a critical anti-oncogenic function for the atonal transcription factor in the fly retina, where atonal instructs tissue differentiation. In the tumor context, atonal acts by regulating cell proliferation and death via the JNK stress response pathway. Combined with evidence that atonal's mammalian homolog, ATOH1, is a tumor suppressor gene, our data support a critical, evolutionarily conserved, function for ato in oncogenesis.

 

【Abstract】

Colon cancer accounts for more than 10% of all cancer deaths annually. Our genetic evidence from Drosophila and previous in vitro studies of mammalian Atonal homolog 1 (Atoh1, also called Math1 or Hath1) suggest an anti-oncogenic function for the Atonal group of proneural basic helix-loop-helix transcription factors. We asked whether mouse Atoh1 and human ATOH1 act as tumor suppressor genes in vivo. Genetic knockouts in mouse and molecular analyses in the mouse and in human cancer cell lines support a tumor suppressor function for ATOH1. ATOH1 antagonizes tumor formation and growth by regulating proliferation and apoptosis, likely via activation of the Jun N-terminal kinase signaling pathway. Furthermore, colorectal cancer and Merkel cell carcinoma patients show genetic and epigenetic ATOH1 loss-of-function mutations. Our data indicate that ATOH1 may be an early target for oncogenic mutations in tissues where it instructs cellular differentiation.