bluuebunny/crossref_metadata_2025_split huggingface dataset:
Bookbuidling, Auctions, and the Future of the IPO Process
Authors: Wilhelm William J. 
Published: April 2005

Auction theorists predict that bookbuilding, long the standard process for selling equity IPOs in the U.S., is about to give way to an Internet‐based IPO auction process that is both more efficient and more fair. The promise of auctions is that, by using an electronic platform that gives all investors the opportunity to bid on IPOs, the underpricing of IPOs and commissions to underwriters will be reduced, leading to an increase in net proceeds to issuers.Largely missing from such arguments, however, is an appreciation of why bookbuilding has dominated U.S. practice (and continues to supplant auctions in IPOs in most countries outside the U.S) and the role of undepricing in the IPO process. Rather than canvassing all investors, bookbuilding involves eliciting expressions of interest from institutional investors, and then allocating shares mainly according to the strength of their professed interest. In contrast to auctions, which allocate shares according to a set of explicit rules, bookbuilding involves a set of implicit “rules” that provide considerable room for judgment by the underwriter. This does not mean that the rules are arbitrary or not well understood by participants, particularly after thousands of IPOs conducted over the better part of two centuries. But to manage the exchange of information between issuers and investors, and the potential conflicts of interest in representing both groups, such rules must be administered by an intermediary with a considerable stake in protecting its reputation for fair dealing. Investment banks that deal with both issuers and the investment community on a regular basis are well positioned to perform this function.The underpricing of IPOs is best viewed not as a transfer of wealth from issuers to favored investors but rather as compensation to the large influential investors that play a major role in the price discovery process. By opening the process to all comers, auctions will discourage these large investors from bidding aggressively because less sophisticated investors will be able to “free ride” on their research and due diligence. To the extent this happens, auctions may suc ceed in reducing underpricing (in fact, they may even lead to over pricing), but they will also reduce the net proceeds for issuers.Nevertheless, recent advances in communications technology and auction theory will undoubtedly reshape current securities underwriting practices. In particular, Internet auctions are likely to replace bookbuilding in debt IPOs and less risky equity issues (say, IPOs of LBOs). But the argument that Bookbuilding will be completely cast aside in favor of largely untested alternatives fails to appreciate a successful institutional response to major market imperfections, some of which can never be wholly eliminated. Especially in the case of risky (first‐time) equity IPOs, there will continue to be an important role for managing the information exchange between issuers and investors that is critical to the IPO process.
Surface Hydrophobicity Changes of Two
Candida albicans
Serotype B
mnn4
Δ Mutants
Authors: Singleton David R. , Masuoka James , Hazen Kevin C. 
Published: April 2005

ABSTRACT

Cell surface hydrophobicity (CSH) of
Candida
species enhances virulence by promoting adhesion to host tissues. Biochemical analysis of yeast cell walls has demonstrated that the most significant differences between hydrophobic and hydrophilic yeasts are found in the acid-labile fraction of
Candida albicans
phosphomannoprotein, suggesting that this fraction is important in the regulation of the CSH phenotype. The acid-labile fraction of
C. albicans
is unique among fungi, in that it is composed of an extended polymer of β-1,2-mannose linked to the acid-stable region of the
N
-glycan by a phosphodiester bond.
C. albicans
serotype A and B strains both contain a β-1,2-mannose acid-labile moiety, but only serotype A strains contain additional β-1,2-mannose in the acid-stable region. A knockout of the
C. albicans
homolog of the
Saccharomyces cerevisiae MNN4
gene was generated in two serotype B
C. albicans
patient isolates by using homologous gene replacement techniques, with the anticipation that they would be deficient in the acid-labile fraction and, therefore, demonstrate perturbed CSH. The resulting
mnn4
Δ-deficient derivative has no detectable phosphate-linked β-1,2-mannose in its cell wall, and hydrophobicity is increased significantly under conditions that promote the hydrophilic phenotype. The
mnn4
Δ mutant also demonstrates an unanticipated perturbation in the acid-stable mannan fraction. The present study reports the first genetic knockout constructed in a serotype B
C. albicans
strain and represents an important step for dissecting the regulation of CSH.
Combinatorial Repression of the Hypoxic Genes of
Saccharomyces cerevisiae
by DNA Binding Proteins Rox1 and Mot3
Authors: Klinkenberg Lee G. , Mennella Thomas A. , Luetkenhaus Katharina , Zitomer Richard S. 
Published: April 2005

ABSTRACT

The hypoxic genes of
Saccharomyces cerevisiae
are transcriptionally repressed during aerobic growth through recruitment of the Ssn6/Tup1 general repression complex by the DNA binding protein Rox1. A second DNA binding protein Mot3 enhances repression of some hypoxic genes. Previous studies characterized the role of Mot3 at the hypoxic
ANB1
gene as promoting synergy among one Mot3 site and two Rox1 sites comprising operator A of that gene. Here we studied the role of Mot3 in enhancing repression by Rox1 at another hypoxic gene,
HEM13
, which is less strongly regulated than
ANB1
and has a very different arrangement of Rox1 and Mot3 binding sites. By assessing the effects of deleting Rox1 and Mot3 sites individually and in combination, we found that the major repression of
HEM13
occurred through three Mot3 sites closely spaced with a single Rox1 site. While the Mot3 sites functioned additively, they enhanced repression by the single Rox1 site, and the presence of Rox1 enhanced the additive effects of the Mot3 sites. In addition, using a Rox1-Ssn6 fusion protein, we demonstrated that Mot3 enhances Rox1 repression through helping recruit the Ssn6/Tup1 complex. Chromatin immunoprecipitation assays indicated that Rox1 stabilized Mot3 binding to DNA. Integrating these results, we were able to devise a set of rules that govern the combinatorial interactions between Rox1 and Mot3 to achieve differential repression.
Contribution of CAF-I to Anaphase-Promoting-Complex-Mediated Mitotic Chromatin Assembly in
Saccharomyces cerevisiae
Authors: Harkness Troy A. A. , Arnason Terra G. , Legrand Charmaine , Pisclevich Marnie G. , Davies Gerald F. , Turner Emma L. 
Published: April 2005

ABSTRACT

The anaphase-promoting complex (APC) is required for mitotic progression and genomic stability. Recently, we demonstrated that the APC is also required for mitotic chromatin assembly and longevity. Here, we investigated the role the APC plays in chromatin assembly. We show that
apc5

CA

mutations genetically interact with the CAF-I genes as well as
ASF1
,
HIR1
, and
HIR2
. When present in multiple copies, the individual CAF-I genes,
CAC1
,
CAC2
, and
MSI1
, suppress
apc5

CA

phenotypes in a CAF-1- and Asf1p-independent manner. CAF-I and the APC functionally overlap, as
cac1Δ cac2Δ msi1Δ
(
caf1Δ
) cells expressing
apc5

CA

exhibit a phenotype more severe than that of
apc5

CA

or
caf1Δ
. The Ts
−
phenotypes observed in
apc5

CA

and
apc5

CA

caf
mutants may be rooted in compromised histone metabolism, as coexpression of histones H3 and H4 suppressed the Ts
−
defects. Synthetic genetic interactions were also observed in
apc5

CA

asf1Δ
cells. Furthermore, increased expression of genes encoding Asf1p, Hir1p, and Hir2p suppressed the
apc5

CA

Ts
−
defect in a CAF-I-dependent manner. Together, these results suggest the existence of a complex molecular mechanism controlling APC-dependent chromatin assembly. Our data suggest the APC functions with the individual CAF-I subunits, Asf1p, and the Hir1p and Hir2p proteins. However, Asf1p and an intact CAF-I complex are dispensable for CAF-I subunit suppression, whereas CAF-I is necessary for
ASF1
,
HIR1
, and
HIR2
suppression of
apc5

CA

phenotypes. We discuss the implications of our observations.
Surface Localization of the Yps3p Protein of
Histoplasma capsulatum
Authors: Bohse Megan L. , Woods Jon P. 
Published: April 2005

ABSTRACT

The
YPS3
gene of
Histoplasma capsulatum
encodes a protein that is both resident in the cell wall and also released into the culture medium. This protein is produced only during the pathogenic yeast phase of infection and is also expressed differently in
H. capsulatum
strains that differ in virulence. We investigated the cellular localization of Yps3p. We demonstrated that the cell wall fraction of Yps3p was surface localized in restriction fragment length polymorphism class 2 strains. We also established that Yps3p released into the G217B culture supernatant binds to the surface of strains that do not naturally express the protein. This binding was saturable and occurred within 5 min of exposure and occurred similarly with live and heat-killed
H. capsulatum
. Flow cytometric analysis of
H. capsulatum
after enzymatic treatments was consistent with Yps3p binding to chitin, a carbohydrate polymer that is a component of fungal cell walls. Polysaccharide binding assays demonstrated that chitin but not cellulose binds to and extracts Yps3p from culture supernatants.
PldB, a Putative Phospholipase D Homologue in
Dictyostelium discoideum
Mediates Quorum Sensing during Development
Authors: Chen Yi , Rodrick Vanessa , Yan Yi , Brazill Derrick 
Published: April 2005

ABSTRACT

Quorum sensing, also known as cell-density sensing in the unicellular eukaryote
Dictyostelium discoideum
, is required for efficient entry into the differentiation and development segment of its life cycle. Quorum sensing is accomplished by simultaneously secreting and sensing the glycoprotein Conditioned Medium Factor, or CMF. When the density of starving cells is high, CMF levels are high, which leads to aggregation followed by development. Here, we describe the role of
pldB
, a gene coding for a putative phospholipase D (PLD) homologue, in quorum sensing. We find that in submerged culture, adding butanol, an inhibitor of PLD-catalyzed phosphatidic acid production, allows cells to bypass the requirement for CMF mediated quorum sensing and aggregate at low cell density. Deletion of
pldB
mimics the presence of butanol, allowing cells to aggregate at low cell density.
pldB
−
cells also initiate and finish aggregation rapidly. Analysis of early developmental gene expression in
pldB
−
cells reveals that the cyclic AMP receptor cAR1 is expressed at higher levels earlier than in wild-type cells, which could explain the rapid aggregation phenotype. As would be predicted, cells overexpressing
pldB
are unable to aggregate even at high cell density. Adding CMF to these
pldB
−
overexpressing cells does not rescue aggregation. Both of these phenotypes are cell autonomous, as mixing a small number of
pldB
−
cells with wild-type cells does not cause the wild-type cells to behave like
pldB
−
cells.
Identification and Gene Expression Analysis of a Large Family of Transmembrane Kinases Related to the Gal/GalNAc Lectin inEntamoeba histolytica
Authors: Beck David L. , Boettner Douglas R. , Dragulev Bojan , Ready Kim , Nozaki Tomoyoshi , Petri William A. 
Published: April 2005

ABSTRACTWe identified in theEntamoeba histolyticagenome a family of over 80 putative transmembrane kinases (TMKs). The TMK extracellular domains had significant similarity to the intermediate subunit (Igl) of the parasite Gal/GalNAc lectin. The closest homolog to theE. histolyticaTMK kinase domain was a cytoplasmic dual-specificity kinase, SplA, fromDictyostelium discoideum. Sequence analysis of the TMK family demonstrated similarities to both serine/threonine and tyrosine kinases. TMK genes from each of six phylogenetic groups were expressed as mRNA in trophozoites, as assessed by spotted oligoarray and real-time PCR assays, suggesting nonredundant functions of the TMK groups for sensing and responding to extracellular stimuli. Additionally, we observed changes in the expression profile of the TMKs in continuous culture. Antisera produced against the conserved kinase domain identified proteins of the expected molecular masses of the expressed TMKs. Confocal microscopy with anti-TMK kinase antibodies revealed a focal distribution of the TMKs on the cytoplasmic face of the trophozoite plasma membrane. We conclude thatE. histolyticaexpresses members of each subgroup of TMKs. The presence of multiple receptor kinases in the plasma membrane offers for the first time a potential explanation of the ability of the parasite to respond to the changing environment of the host.
Pairwise Knockdowns of cdc2-Related Kinases (CRKs) in
Trypanosoma brucei
Identified the CRKs for G
1
/S and G
2
/M Transitions and Demonstrated Distinctive Cytokinetic Regulations between Two Developmental Stages of the Organism
Authors: Tu Xiaoming , Wang Ching C. 
Published: April 2005

ABSTRACT

Expression of the cdc2-related kinase 3 (CRK3) together with expression of CRK1, -2, -4, or -6, were knocked down in pairs in the procyclic and bloodstream forms of
Trypanosoma brucei
, using the RNA interference technique. Double knockdowns of CRK3 and CRK2, CRK4, or CRK6 exerted significant growth inhibition and enriched the cells in G
2
/M phase, whereas a CRK3 plus CRK1 (CRK3 + CRK1) knockdown arrested cells in both G
1
/S and G
2
/M transitions. Thus, CRK1 and CRK3 are apparently the kinases regulating the G
1
/S and G
2
/M checkpoint passages, respectively, whereas the other CRKs are probably playing only minor roles in cell cycle regulation. A CRK1 + CRK2 knockdown in the procyclic form was found to cause aberrant posterior cytoskeletal morphogenesis (X. M. Tu and C. C. Wang, Mol. Biol. Cell
16:
97-105, 2005). A CRK3 + CRK2 knockdown, however, did not lead to such a change, suggesting that CRK2 depletion can lead to the abnormal morphogenesis only when procyclic-form cells are arrested in the G
1
phase. The G
2
/M-arrested procyclic form produces up to 20% stumpy anucleated cells (zoids) in the population, suggesting that cytokinesis and cell division are not blocked by mitotic arrest but are apparently driven to completion by the kinetoplast cycle. In the bloodstream form, however, G
2
/M arrest resulted in little zoid formation but, instead, enriched a population of cells each containing multiple kinetoplasts, basal bodies, and flagella and an aggregate of multiple nuclei, indicating failure in entering cytokinesis. The two different cytokinetic regulations between two distinct stage-specific forms of the same organism may provide an interesting and useful model for further understanding the evolution of cytokinetic control among eukaryotes.
Intracellular Role of Adenylyl Cyclase in Regulation of Lateral Pseudopod Formation duringDictyosteliumChemotaxis
Authors: Stepanovic Vesna , Wessels Deborah , Daniels Karla , Loomis William F. , Soll David R. 
Published: April 2005

ABSTRACTCyclic AMP (cAMP) functions as the extracellular chemoattractant in the aggregation phase ofDictyosteliumdevelopment. There is some question, however, concerning what role, if any, it plays intracellularly in motility and chemotaxis. To test for such a role, the behavior of null mutants ofacaA, the adenylyl cyclase gene that encodes the enzyme responsible for cAMP synthesis during aggregation, was analyzed in buffer and in response to experimentally generated spatial and temporal gradients of extracellular cAMP.acaA−cells were defective in suppressing lateral pseudopods in response to a spatial gradient of cAMP and to an increasing temporal gradient of cAMP.acaA−cells were incapable of chemotaxis in natural waves of cAMP generated by majority control cells in mixed cultures. These results indicate that intracellular cAMP and, hence, adenylyl cyclase play an intracellular role in the chemotactic response. The behavioral defects ofacaA−cells were surprisingly similar to those of cells of null mutants ofregA, which encodes the intracellular phosphodiesterase that hydrolyzes cAMP and, hence, functions opposite adenylyl cyclase A (ACA). This result is consistent with the hypothesis that ACA and RegA are components of a receptor-regulated intracellular circuit that controls protein kinase A activity. In this model, the suppression of lateral pseudopods in the front of a natural wave depends on a complete circuit. Hence, deletion of any component of the circuit (i.e., RegA or ACA) would result in the same chemotactic defect.
Systematic Deletion Analysis of Fission Yeast Protein Kinases
Authors: Bimbó Andrea , Jia Yonghui , Poh Siew Lay , Karuturi R. Krishna Murthy , den Elzen Nicole , Peng Xu , Zheng Liling , O'Connell Matthew , Liu Edison T. , Balasubramanian Mohan K. , Liu Jianhua 
Published: April 2005

ABSTRACT

Eukaryotic protein kinases are key molecules mediating signal transduction that play a pivotal role in the regulation of various biological processes, including cell cycle progression, cellular morphogenesis, development, and cellular response to environmental changes. A total of 106 eukaryotic protein kinase catalytic-domain-containing proteins have been found in the entire fission yeast genome, 44% (or 64%) of which possess orthologues (or nearest homologues) in humans, based on sequence similarity within catalytic domains. Systematic deletion analysis of all putative protein kinase-encoding genes have revealed that 17 out of 106 were essential for viability, including three previously uncharacterized putative protein kinases. Although the remaining 89 protein kinase mutants were able to form colonies under optimal growth conditions, 46% of the mutants exhibited hypersensitivity to at least 1 of the 17 different stress factors tested. Phenotypic assessment of these mutants allowed us to arrange kinases into functional groups. Based on the results of this assay, we propose also the existence of four major signaling pathways that are involved in the response to 17 stresses tested. Microarray analysis demonstrated a significant correlation between the expression signature and growth phenotype of kinase mutants tested. Our complete microarray data sets are available at
http://giscompute.gis.a-star.edu.sg/∼gisljh/kinome
.
Maternal Inheritance and Stage-Specific Variation of the Apicoplast in
Toxoplasma gondii
during Development in the Intermediate and Definitive Host
Authors: Ferguson David J. P. , Henriquez Fiona L. , Kirisits Michael J. , Muench Stephen P. , Prigge Sean T. , Rice David W. , Roberts Craig W. , McLeod Rima L. 
Published: April 2005

ABSTRACT

The structure and location of
Toxoplasma gondii
apicoplasts were examined in intermediate and definitive hosts and shown to vary in a stage-specific manner. Immunocytochemistry and electron microscopy studies were used to identify changes in the morphology of apicoplasts and in their enoyl reductase (ENR) content during asexual and sexual development. Apicoplasts in tachyzoites were small, multimembraned organelles anterior to nuclei that divided and segregated with the nuclei during endodyogeny. In nonproliferating bradyzoites within mature tissue cysts (1 to 24 months), apicoplasts had high levels of ENR. During coccidian development, asexual multiplication (endopolygeny), resulting in simultaneous formation of up to 30 daughters (merozoites), involved an initial growth phase associated with repeated nuclear divisions during which apicoplasts appeared as single, elongated, branched structures with increased levels of ENR. At initiation of merozoite formation, enlarged apicoplasts divided simultaneously, with constrictions, into portions that segregated to developing daughters. In sexual stages, apicoplast division did not occur during microgametogony, and apicoplasts were absent from the microgametes that were formed. In contrast, during macrogametogony, the apicoplast appeared as a large, branched, perinuclear structure that had very high levels of ENR in the absence of nuclear division. Marked increases in the size of apicoplasts and levels of ENR may be related to requirements of the macrogametocytes to synthesize and store all components necessary for oocyst formation and subsequent extracellular sporulation. Thus, it is shown that apicoplasts are present and contain ENR in all
T. gondii
life cycle stages except microgametes, which will result in maternal inheritance of the organelle.
Proteomic Analysis of Phagocytosis in the Enteric Protozoan Parasite
Entamoeba histolytica
Authors: Okada Mami , Huston Christopher D. , Mann Barbara J. , Petri William A. , Kita Kiyoshi , Nozaki Tomoyoshi 
Published: April 2005

ABSTRACT

Proteomic analysis of phagosomes isolated from
Entamoeba histolytica
by liquid chromatography and mass spectrometry identified 85 proteins involved in surface recognition, actin cytoskeleton rearrangement, vesicular trafficking, and degradation. Phagosome localization of representative proteins was verified by immunofluorescence assay. This study should provide a basis for molecular identification and characterization of phagosome biogenesis.
The Highly Conserved tRNA
His
Guanylyltransferase Thg1p Interacts with the Origin Recognition Complex and Is Required for the G
2
/M Phase Transition in the Yeast
Saccharomyces cerevisiae
Authors: Rice Terri S. , Ding Min , Pederson David S. , Heintz Nicholas H. 
Published: April 2005

ABSTRACT

Here we show that the
Saccharomyces cerevisiae
tRNA
His
guanylyltransferase Thg1p interacts with the origin recognition complex in vivo and in vitro and that overexpression of hemagglutinin-Thg1p selectively impedes growth of
orc2
-
1
(Ts) cells at the permissive temperature. Studies with conditional mutants indicate that Thg1p couples nuclear division and migration to cell budding and cytokinesis in yeast.
METHOD FOR DETERMINING THE LOCALIZATION OF TRACE ELEMENTS OBSERVED BY THE MICRO PIXE CAMERA
Authors: HARADA SATOSHI , ISHII K. , TANAKA A. , SATOH T. , MATSUYAMA S. , YAMAZAKI H. , KAMIYA T. , SAKAI T. , ARAKAWA K. , SAITOH M. , OIKAWA S. , SERA K. 
Published: April 2005

The method to observe the localization of the trace elements in cultured human cell, by the micro Particle Induced X-ray Emission (PIXE) camera, was developed. The analyzed samples received the eosin staining, which colored the nucleus of cell violet. The scanned areas of the sample with particle irradiation were colored brown by the heat during irradiation. The brown scanned areas were examined by an optical microscope at 400 X magnification and photographed. Then the photo was digitized and loaded into the microcomputer. By microcomputer, the photo of the scanned area was superimposed onto the image of the micro PIXE camera, by matching the scanned area to the image of micro PIXE camera. This superimposed image enabled us to determine whether the elements exists in cytosol, or in nucleus.