Author Archives: erik
I came across a tweet from IDT with a link to DNA drawings made by some pretty formidable scientists while at a meeting at Cold Spring Harbor in 1993. This list includes Iowa City native and Nobel laureate Tom Cech as well as recognizable names like Brenner, Capecchi, Collins, Greider, Lander (drawing shown here), Paabo, Watson and others. Here’s the link.
I found this website which will hopefully be good resource for finding those difficult to locate papers that are essential references for our manuscripts. This site finds the obscure research articles such as: ‘Zipper release’, naval fluff and boogers (yay for peer review). Here is a background piece on the website.
As mentioned previously, Ahmed Moustafa had his manuscript accepted by Science and it has recently been posted online. This work provides insight into the evolution of diatoms (pics here and here) and provides unexpected analytical data from their genome, shedding light into a convoluted evolution. A perspective was also published in the same issue of Science providing some background and commentary on Ahmed’s paper. Huge congrats to you Ahmed, nice job!
From Ahmed: Although the world’s oceans are currently dominated by phytoplankton such as diatoms and dinoflagellates that contain photosynthetic organelles (plastids) stolen from red algae, it was not always this way. Before the great end Permian extinction about 250 million years ago, the ocean was green, dominated by prasinophyte and other green algae. A clue to this major shift in the algal flora was provided by the recent comparative genome analysis by Moustafa et al. of two diatom species, Thalassiosira and Phaeodactylum. Using a phylogenomic pipeline designed and built in the Bhattacharya lab at the University of Iowa, the authors determined the origin of all 11,000 genes in each of these taxa. This work shows surprisingly that about 1,800 genes in each taxon are of green algal origin. This result provides strong evidence that diatoms and other marine phytoplankton that currently harbor a red algal derived plastid once contained a green algal endosymbiont that provided these “hidden” genes to their genome. This ancient cryptic endosymbiosis, rather than being an oddity, appears to have outfitted chromalveolates with genes from two taxonomically distantly related groups (green, followed by red algae), allowing them to complement their genetic potential. Many of the retained green genes provide key functions to chromalveolates such as enhanced photoprotection and a host of metabolite transporters to more effectively use dissolved nutrients in the environment, whereas many others likely have equally important but currently unknown functions. These data may therefore help to explain the rise to dominance of chromalveolates in the oceans. The work also reveals the genomic gymnastics that have occurred over millions of years in the marine environment resulting in highly chimeric nuclear genomes shaped by serial endosymbiosis.
Click journal image for link.
Lea Davis, Kacie Meyer, Danielle Rudd
Ahmed Moustafa and Alissa Hulstrand will be presenting @ Student Seminar this week on the eastside of campus in 106 BBE @ noon. As usual, I have asked the speakers to provide some background information for their talks. Hope to see you all there.
Background for Ahmed’s Talk
Diatoms and other chromalveolates are among the dominant phytoplankton in the world’s oceans. Endosymbiosis was essential to the success of chromalveolates and it appears the ancestral plastid in this group of red algal originated via a single, ancient secondary endosymbiosis. However, recent analyses have turned up a handful of nuclear genes in chromalveolates that are of green algal derivation. Using a genome-wide approach to estimate the “green” contribution to diatoms, we identified >1,700 green gene transfers, comprising 16% of the diatom nuclear coding potential. These genes were likely introduced into diatoms and other chromalveolates from a cryptic endosymbiont related to prasinophyte-like green algae. Chromalveolates appear to have recruited genes from the two major existing algal groups to forge a highly successful, species-rich protist lineage.
Focuses on the functional genomics of harmful algae (Red Tide) and evolutionary genomics of marine microalgae. Working on characterizing and determining the origin and assembly of the saxitoxin gene cluster in cyanobacteria. Also, profiling global gene expression patterns in dinoflagellates and the impact of bacterial interaction on the transcriptional regulation in dinoflagellates.
Background for Alissa’s Talk
Many cellular functions, such as axis determination and cell movement, are dependent on the asymmetrical distribution of proteins and RNAs. In Xenopus laevis, several maternal mRNAs essential for normal development are localized to the oocyte vegetal cortex, and our lab has used microarrays to identify numerous additional localized RNAs. In this work we characterize one of these cortex-enriched transcripts, cep4l. CEP4L belongs to a family of Cdc42 effector proteins (CEPs) that bind Cdc42 and related small GTPases, which can regulate the actin cytoskeleton. Using in situ hybridization we found that cep4l is expressed in the oocyte vegetal cortex and throughout embryonic development. The embryonic expression pattern includes migratory cell populations during gastrulation and neurulation, and neural regions in older embryos. To begin to ascertain the function of cep4l in development we misexpressed cep4l RNA in embryos. We found that this overexpression causes convergent extension defects, cell disaggregation, and induces ectopic neural and neuronal marker expression, indicating a potential role in neurogenesis. Structure-function analyses using deletion mutant constructs show a role for the CRIB domain, a conserved GTPase binding domain. We also present loss of function data showing a role for cep4l in normal axial and nervous system development. Although the roles of small GTPases in cell migration and adhesion are well-characterized, our results suggest novel roles for these proteins and their effectors in neurogenesis and early development.
The votes are in and Pamela will be taking over as the Student Representative position to the Executive Committee in the near future. Thanks to all of you who voted.
We will have Student Seminar this Thursday @ noon in 2289 CBRB. Shyam Ramachandran will present his current research on Thursday in 2289 CBRB and has provided the following background for his talk.
In cystic fibrosis (CF; OMIM), the lungs are particularly susceptible to infection, with concomitant inflammation and alteration in airway morphology. It is widely believed that the pulmonary disease pathology of CF is a result of the complex interplay between innate immunity, infection and inflammation at the epithelial surface. The focus of my talk will be to provide an update of the different projects involved in answering some fundamental questions plaguing the CF community. I will touch upon latest data from mRNA-expression profiling and microRNA deep sequencing from the human and pig model of CF, and try to highlight what we have learnt and the directions we wish to take further on.
Robert Weinberg (founding member of Whitehead, founder of 1st oncogene [Ras] and tumor supressor [RB]; National Medal of Science; PubMed, Wikipedia), one of the premier scientists in cancer biology and genetics will be giving a talk today (Friday, April 17th) on the east side of the Iowa river in C20 Pomerantz Center (Map) @ 4pm. He is a major player in cancer research and I’m sure will give an interesting review of the state of cancer research as it stands today and hopefully some of his current research.
Student Seminar is upon us again and we will have Pamela Pretorius and Patricia Schneider presenting on Thursday @ noon in 2289 CBRB. As usual I have asked them both to provide me some background information to bring us all up to speed regarding their past research. See you Thursday.
Visual impairment and blindness have far reaching implications for society. In 2002, a study by the World Health Organization (WHO) found that 161 million people worldwide suffered from visual impairment, making vision loss and blindness not only a personal burden but also a global burden. Hundreds of individually rare, but collectively common Mendelian disorders can cause blindness. One of those disorders is a heterogeneous syndromic form of retinal degeneration, Bardet-Biedl Syndrome (BBS). A pleiotropic disorder, BBS is characterized by obesity, retinitis pigmentosa, polydactyly, renal abnormalities, hypogenitalism and cognitive impairment. In addition, BBS is also associated with an increased susceptibility to hypertension, diabetes mellitus and heart defects. Although BBS is a rare disorder in the general population, some components of the BBS phenotype, such as obesity, diabetes and blindness, are common in the general population. BBS is a syndromic form of retinitis pigmentosa (RP). A syndromic form of retinitis pigmentosa (RP), individuals with BBS experience central vision loss during childhood or early adolescence and are blind by the second or third decade of life.
Our lab has established both the mouse and zebrafish as models to further study both cellular and molecular events underlying this retinal degeneration. We have generated five knockout lines as well as a knockin mouse for BBS and all recapitulate the human BBS phenotype of retinal degeneration. Interestingly, death of the photoreceptors is preceded by mislocalization of rhodopsin, suggesting that there is a defect in intracellular transport in Bbs mutant mice. Additionally, we have adapted a cone-based vision assay to test visual acuity in the zebrafish.
The focus of my project is to evaluate the molecular and biological processes behind the retinal degeneration observed in the human disease Bardet-Biedl Syndrome (BBS) with respect to two BBS3 (NCBI, UCSC) transcripts.
Background for Patricia’s Presentation:
I have a special interest in understanding how Wnt signaling controls the formation of the embryonic axis in vertebrates. I use the zebrafish and Xenopus laevis to unravel the mechanisms behind axis formation. In our lab, we utilize gene knockdown as well as transgenic lines to dissect the function of members of this signaling pathway during embryonic stages.
The Wnt signaling network has critical roles in cell proliferation, differentiation morphogenesis and stem cell biology. Complexity of the Wnt signaling network is apparent in early embryonic development. For instance, activation of maternal Wnt signaling is essential for dorsal specification, whereas inhibition of zygotic Wnt signaling is required for patterning of the anterior-posterior axis. Modulation of β-catenin protein levels is central to the function of Wnt signaling. In the absence of a class of Wnt ligands, a degradation complex including Axin, adenomatous polyposis coli (APC) and glycogen synthase kinase 3 (GSK3) stimulates the phosphorylation and degradation of β-catenin. In the presence of a class of Wnt ligands, Dishevelled (Dsh) protein is activated, recruits Axin to the plasma membrane and inhibits the degradation complex, allowing β-catenin to accumulate. β-catenin can then translocate to the nucleus interact with cofactors and activate transcription.
Axin is a key player in the degradation complex, as it serves as the scaffold for proteins involved in the phosphorylation of β-catenin. Axin contains four critical domains: a β-catenin binding domain, a GSK3 binding domain, a Regulator of G-protein (RGS) domain and a DIX domain (protein interaction domain shared with Dsh). RGS domains are typical of RGS proteins, which were originally identified as regulators of the active half-life of G-protein signaling. However, it is not known whether the Axin-RGS domain functions in G-protein signaling. My work focuses on the function of the Axin-RGS domain during maternal and zygotic stages.