Division Of Biology Research Articles

In vitro Studies of the Antibody Response: Antibodies of Different Specificity are Made in Different Populations of Cells.

In vitro Studies of the Antibody Response: Antibodies of Different Specificity are Made in Different Populations of Cells.

FRESHWATER ROTIFER: (PART II) A LABORATORY STUDY OF NATIVE FRESHWATER ROTIFERS Brachionus angularis AND B. quadridentatus brevispinus FROM TABASCO

This study is a first report of rotifer form the South of Mexico. The rotifers were collected from the fishponds arround Biological Division, UJAT and we examined their morphometric characters, cultivated and identified them. We conducted experiment at different salt concentrations tested at 0g L–1 water (no add NaCL), 2g L–1, 4g L–1, 6g L–1, 8g L–1, 10g L–1 water. The species were identified as Brachionus angularis Gosse (1851) characterized by having two anterior spines, which are almost invisible while B. quadridentatus brevispinus Ehrenberg (1832) with six anterior spines, which can be seen clearly. Lorica size of B. angularis and B. quadridentatus brevispinus are about 12.14 and 12.8 m, respectively and the size is much smaller than B. plicatilis (Mazatlan strain).

Mutational analysis of genes coding for cell surface proteins in colorectal cancer cell lines reveal novel altered pathways, druggable mutations and mutated epitopes for targeted therapy.

We carried out a mutational analysis of 3,594 genes coding for cell surface proteins (Surfaceome) in 23 colorectal cancer cell lines, searching for new altered pathways, druggable mutations and mutated epitopes for targeted therapy in colorectal cancer. A total of 3,944 somatic non-synonymous substitutions and 595 InDels, occurring in 2,061 (57%) Surfaceome genes were catalogued. We identified 48 genes not previously described as mutated in colorectal tumors in the TCGA database, including genes that are mutated and expressed in >10% of the cell lines (SEMA4C, FGFRL1, PKD1, FAM38A, WDR81, TMEM136, SLC36A1, SLC26A6, IGFLR1). Analysis of these genes uncovered important roles for FGF and SEMA4 signaling in colorectal cancer with possible therapeutic implications. We also found that cell lines express on average 11 druggable mutations, including frequent mutations (>20%) in the receptor tyrosine kinases AXL and EPHA2, which have not been previously considered as potential targets for colorectal cancer. Finally, we identified 82 cell surface mutated epitopes, however expression of only 30% of these epitopes was detected in our cell lines. Notwithstanding, 92% of these epitopes were expressed in cell lines with the mutator phenotype, opening new venues for the use of "general" immune checkpoint drugs in this subset of patients.

Gauging Satisfaction with the New Proposal Process in DEB and IOS at the NSF

The Division of Environmental Biology (DEB) and the Division of Integrative Organismal Systems (IOS) at the National Science Foundation recently made three key changes to the core program review process: a new preliminary proposal requirement, a cap on the number of proposals that principal investigators (PIs) submit per cycle, and a switch to an annual deadline. We queried the scientific community on their level of satisfaction with key facets of the new system and their perception of the consequences. We received 4736 responses (a 24% response rate). Our results show that there was no qualitative difference in reported satisfaction between the PIs in DEB and IOS. The preliminary proposal requirement was viewed most favorably, and the switch to a single annual deadline elicited the most dissatisfaction. Continued monitoring of these early trends through time will be important to ensure that funds are allocated fairly in support of the best science.

Oncolytic viruses targeting tumor stem cells.

A workshop "Targeting Oncolytic Viruses to Tumor Stem Cells," organized by the Division of Cancer Biology, NCI, NIH, was held on September 6, 2013 in Rockville, MD. Seventeen invited experts presented an overview of their current research in this area and discussed the state of current research on the use of oncolytic viruses targeted to stem cells as a potential cancer therapy. The goal was to evaluate the evidence that this approach might increase the efficacy of oncolytic virus therapy and to identify gaps in knowledge that have retarded progress in this area.

Imagining black America

Scientific research has now established that race should be understood as a social construct, not a true biological division of humanity. In Imagining Black Michael Wayne explores the construction and reconstruction of black America from the arrival of the first Africans in Jamestown in 1619 to Barack Obama's reelection. Races have to be imagined into existence and constantly reimagined as circumstances change, Wayne argues, and as a consequence the boundaries of black America have historically been contested terrain. He discusses the emergence in the nineteenth century--and the erosion, during the past two decades--of the notorious one-drop rule. He shows how significant periods of social transformation--emancipation, the Great Migration, the rise of the urban ghetto, and the Civil Rights Movement--raised major questions for black Americans about the defining characteristics of their racial community. And he explores how factors such as class, age, and gender have influenced perceptions of what it means to be black. Wayne also considers how slavery and its legacy have defined freedom in the United States. Black Americans, he argues, because of their deep commitment to the promise of freedom and the ideals articulated by the Founding Fathers, became and remain quintessential Americans--the incarnation of America, in the words of the civil rights leader A. Philip Randolph.

What is the future potential of the PI3K pathway in colorectal cancer treatment?

Systems Biology & Personalised Medicine Division, Walter & Eliza Hall Institute of Medical Research, Parkville, Victoria, Australia Faculty of Medicine, Dentistry & Health Sciences, Department of Medical Biology, University of Melbourne, Parkville, Victoria, Australia Department of Medical Oncology, Royal Melbourne Hospital, Parkville & Western Hospital, Footscray, Victoria, Australia *Author for correspondence: oliver.sieber@ludwig.edu.au Therapeutic options for treating patients with metastatic colorectal cancer (CRC) have increased markedly over the past decade. Recent improvements in overall survival rates from 10 to 24 months have been achieved through the introduction of molecularly targeted agents to complement traditional cytotoxics, including agents directed against the EGF receptor (EGFR) pathway (cetuximab and panitumumab) and angiogenesis (bevacizumab, aflibercept and regorafenib). This progress has spurred intense efforts to develop further compounds that target key molecular pathways driving carcinogenesis. One major focus has been on the inhibition of oncogenic PI3K signaling, with diverse inhibitors currently in Phase I/II clinical trials. While achieving clear responses in some cancers, activity in CRC has been modest, with disease stabilization observed in approximately 10% of patients. Here, we discuss the potential opportunities of targeting the PI3K pathway in treating patients with metastatic CRC. PI3K/AKT signaling is typically initiated via growth factors (e.g., EGF) or insulin, resulting in activation of receptor tyrosine kinases or G-protein coupled receptors. Activated receptor tyrosine kinases/G-protein coupled receptors recruit and activate class IA PI3K at the cell membrane, enabling PI3K to convert PIP2 to PIP3. PIP3 recruits the serene–threonine protein kinase AKT, which is rendered fully active through phosphorylation by PDK1 and mTORC2. Phosphorylated AKT transduces the signal to a range of downstream substrates (e.g., NF-κB, TSC1/2 complex, mTORC1, S6K, 4EBP1, BAD, GSK3β and MDM2) affecting cell proliferation, growth, survival, apoptosis, protein synthesis and glucose metabolism [1]. PI3K signaling is negatively regulated by the PTEN phosphatase, which removes the 3-phosphate from PIP3. In addition, PI3K can be stimulated by GTP-bound RAS, a crosstalk important for RAS mutation-induced transformation of mammalian cells. Michelle Palmieri1,2, Jayesh Desai1,3 & Oliver Sieber*,1

Regulation of mitochondrial fission by MiD51 (757.1)

Regulation of mitochondrial fission by MiD51 Oliver C. Losόn1, Michael E. Rome1, Jens T. Kaiser2, Shu‐ou Shan2 and David C. Chan1,3 1Division of Biology and Biological Engineering, 2Division of Chemistry and Chemical Engineering and 3Howard Hughes Medical Institute, California Institute of Technology, Pasadena CA, 91125, USA Mitochondrial fission requires the recruitment of dynamin‐related protein 1 (Drp1) to mitochondria and activation of its GTP‐dependent scission function. In mammals, the recruitment of Drp1 is primarily regulated by the outer membrane receptors Mff, MiD49 and MiD51, while Fis1 plays a minor role. We recently demonstrated that these receptors can function independently of one another to recruit Drp1 and mediate mitochondrial division. Intriguingly, exogenous expression of MiD49 and MiD51 causes constitutive recruitment of Drp1 but inhibits its scission activity. With mitochondrial stress, however, these receptors can rapidly activate pre‐recruited Drp1 and cause rapid mitochondrial fragmentation independently of Fis1 and Mff. This behavior suggests an ability to sense mitochondrial function, but the molecular mechanism is unknown. To better understand the role of the MiDs in regulating mitochondrial fission, we produced recombinant protein pertaining to the cytosolic domain of each MiD, and performed crystallographic screens. We obtained crystals for MiD51 that diffracted to high resolution, and we were able to determine its structure. MiD51 possesses a nucleotidyl transferase fold and uses a variant set of residues to tightly bind a ligand. We have performed a structure‐function analysis of MiD51 by mutating structurally implicated residues and studying their importance in vivo and in vitro to activate Drp1. Our analysis reveals how MiD51 activates mitochondrial fission during mitochondrial stress.

The Escherichia coli Tol‐Pal complex is essential for the positioning of proteins at the cell poles (948.3)

Organisms regulate essential biological processes, including growth, division, motility, and virulence, by controlling the subcellular localization of proteins and other biomolecules. Even though bacterial cells lack a complex internal system of endomembrane, they use numerous mechanisms to establish, maintain and replicate their subcellular organization. Particularly, the bacterial poles are home to numerous cytoplasmic and membrane proteins. However, the molecular mechanisms regulating the non‐uniform localization of polar proteins are largely unknown. Here we show that the Tol−Pal complex_a conserved component that maintains cell wall integrity in Gram‐negative bacteria_plays a key role in the polar localization of chemoreceptors in Escherichia coli. Mutants lacking the Tol−Pal complex and expressing fluorescently labeled chemoreceptors showed characteristically mis‐localized (i.e., non‐polar) chemoreceptors dispersed along the length of the cells. Cell motility and chemotaxis assays showed that the mutants presented motility and chemosensory defects that were not observed in the wild‐type strain. My long term goal is to investigate the role of the Tol−Pal complex in a diverse group of bacteria, with a focus on bio‐medically relevant organisms.Grant Funding Source: Supported by National Institute of Health (1DP2OD008735‐01)

ECS Organic & Biological Electrochemistry Division Manuel M. Baizer Award C-H Amination of Aromatic Compounds Based on Electrochemical Oxidation

We have developed a new method for synthesizing aromatic primary amines from aromatic compounds based on electrochemical oxidation of aromatic compounds in the presence of pyridine followed by the reaction of the resulting N-arylpyridinium ions with an alkylamine. This transformation serves as a powerful method for C−H amination of aromatic compounds without using metal catalysts and harsh chemical reagents. Synthetic utility of the method is demonstrated by C−H amination of aromatic compounds bearing a nitro group to give a key intermediate for the synthesis of bioactive compounds such as a VLA-4 antagonist.

Modelling calcium-dependent proteins in the spine - challenges and solutions

Event Abstract Back to Event Modelling calcium-dependent proteins in the spine - challenges and solutions Melanie I. Stefan1*, Shirley Pepke1, Stefan Mihalas1, Thomas Bartol2, Terrence Sejnowki2 and Mary B. Kennedy1 1 California Institute of Technology, Biology Division, United States 2 Salk Institute, United States Synaptic plasticity is mediated by calcium signalling in the postsynaptic spine. One hypothesis suggests that the direction of plasticity is determined by the relative activation of two Ca2+-/calmodulin dependent proteins, CaMKII and calcineurin [Lisman. PNAS, 1989], and the subsequent activation of tightly regulated signalling pathways in the spine. Computational modelling allows us to gain an insight into how proteins within this complex signalling pathway may be regulated and in turn regulate each other. It can also improve understanding of its complex and often non-intuitive behaviour under varying conditions. Three features of this signalling system pose a challenge to computational modellers: First, the absolute number of molecules in a dendritic spine is small, which makes reactions stochastic and affects competition between proteins. Second, the constrained geometry within the dendritic spine affects diffusion and creates distinct, dynamic signalling microdomains. Third, the large number of possible modifications on signalling proteins such as CaMKII increases combinatorial complexity and requires modelling strategies that can work with large numbers of possible states. To manage all three of these challenges, we are using the spatial stochastic simulator MCell [Kerr et al. SIAM J Sci Comput, 2008]. MCell is an agent-based Monte-Carlo simulator that allows stochastic modelling in arbitrarily complex geometries. It is therefore ideally suited to model systems with small molecule numbers and spatial constraints. A realistic reconstruction of a portion of a dendrite has recently been used for modelling calcium transients within CA1 neurons using MCell [Keller et al. submitted]. We are currently combining this technology with an earlier kinetic model of calmodulin activation by calcium [Pepke et al. PLoS Comput Biol, 2010] to explore the relationship between calcium signalling, calmodulin activation and the regulation of calmodulin targets in the spine. As an agent-based simulator, MCell allows for simulation of multistate signalling systems which are so complex as to be intractable using ODE/PDE or the Gillespie algorithm. This allows us to use MCell to construct a detailed model of CaMKII activation that includes all the complexities of calmodulin binding [Stefan et al. PLoS ONE, 2012], phosphorylation [Miller and Kennedy. Cell, 1986], conformational change and intramolecular regulation [Chao et al. Nat Struct Mol Biol, 2010]. Keywords: computational neuroscience, modelling, Calcium signalling, calcium dependent proteins, computational modeling Conference: 5th INCF Congress of Neuroinformatics, Munich, Germany, 10 Sep - 12 Sep, 2012. Presentation Type: Poster Topic: Neuroinformatics Citation: Stefan M, Pepke S, Mihalas S, Bartol T, Sejnowki T and Kennedy M (2014). Modelling calcium-dependent proteins in the spine - challenges and solutions. Front. Neuroinform. Conference Abstract: 5th INCF Congress of Neuroinformatics. doi: 10.3389/conf.fninf.2014.08.00091 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 21 Mar 2013; Published Online: 27 Feb 2014. * Correspondence: Dr. Melanie I. Stefan, California Institute of Technology, Biology Division, Pasadena, United States, mstefan@caltech.edu Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Melanie I. Stefan Shirley Pepke Stefan Mihalas Thomas Bartol Terrence Sejnowki Mary B. Kennedy Google Melanie I. Stefan Shirley Pepke Stefan Mihalas Thomas Bartol Terrence Sejnowki Mary B. Kennedy Google Scholar Melanie I. Stefan Shirley Pepke Stefan Mihalas Thomas Bartol Terrence Sejnowki Mary B. Kennedy PubMed Melanie I. Stefan Shirley Pepke Stefan Mihalas Thomas Bartol Terrence Sejnowki Mary B. Kennedy Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.

Lawrence D. Longo: from chronic fetal hypoxia to proteomic predictors of fetal distress syndrome - a life devoted to research and mentoring based on virtue-ethics.

The present chapter presents the experience of the author during his fellowship granted by the Fogarty Foundation of the NIH in the Division of Perinatal Biology, Loma Linda University, from 1989 to 1991. Experiments on maternal and fetal responses to long-term hypoxemia (including high-altitude) were performed successfully in pregnant sheep and their fetuses.Cardiovascular, hormonal and blood flow distribution responses were studied under a strict experimental protocol. As result of this research, four papers were accepted for publication in major scientific journals, and have served as basis for further research.Most of all, the leadership, virtue-based ethics, perseverance and continuous stimulus of Lawrence D. Longo is presented as an example to follow for future generations.

Morphological comparisons of metacarpal I for Australovenator wintonensis and Rapator ornitholestoides: implications for their taxonomic relationships

WHITE, M.A., FALKINGHAM, P.L., COOK, A.G., HOCKNULL, S.A. & ELLIOTT, D.A., 2013. Morphological comparisons of metacarpal I for Australovenator wintonensis and Rapator ornitholestoides: implications for their taxonomic relationships. Alcheringa 37, 1 - 7. ISSN 0311-5518.Various comparisons of left metacarpal I of the Australovenator wintonensis holotype have been made with Rapator ornitholestoides. These specimens were identified as being morphologically more similar than either was to that of the neovenatorid Megaraptor namunhuaiquii. Owing to the poor preservation of A. wintonensis and R. ornitholestoides, distinct morphological separation between the two appeared minimal. The recent discovery of a near perfectly preserved right metacarpal I of A. wintonensis enables a direct and accurate comparison with R. ornitholestoides. Distinct morphological differences exist between the metacarpals of the two species. A re-evaluation of the age of the A. wintonensis holotype site (AODL 85 ‘Matilda Site’) with zircon dating reveals a maximum age of 95 Ma, 10 Ma younger than the Griman Creek Formation at Lightning Ridge, from which R. ornitholestoides was recovered. This age difference detracts from the probability that the specimens belong to the same genus.Matt A. White∗ [fossilised@hotmail.com], School of Engineering, The University of Newcastle, Callaghan, New South Wales 2308, Australia; Peter L. Falkingham† [pfalkingham@rvc.ac.uk], Department of Comparative Biomedical Sciences, Structure and Motion Laboratory, Royal Veterinary College, London, UK; Alex G. Cook [alex.cook@y7mail.com] and Scott A. Hocknull [scott.hocknull@qm.qld.gov.au], Ancient environments, Queensland Museum, Hendra, Queensland, 4011, Australia; David A. Elliott [david.elliott@aaod.com.au], Australian Age of Dinosaurs Museum of Natural History, The Jump Up, Winton, Queensland, 4735, Australia. ∗Also affiliated with Australian Age of Dinosaurs Museum of Natural History, The Jump Up, Winton, Queensland 4735, Australia. †Also affiliated with Department of Ecology and Evolutionary Biology, Division of Biology and Medicine, Brown University, USA. Received 22.9.2012; revised 13.1.2013; accepted 17.1.2013.

Editorial introductions

Editorial introductions

Departments Can Develop Teaching Identities of Graduate Students

Departments Can Develop Teaching Identities of Graduate Students

Combining TRAIL with PI3 Kinase or HSP90 inhibitors enhances apoptosis in colorectal cancer cells via suppression of survival signaling

TRAIL has been shown to induce apoptosis in cancer cells, but in some cases they fail to respond to this ligand. We explored the ability of representative phosphatidylinositol-3-kinase (PI3 Kinase)/mTOR and HSP90 inhibitors to overcome TRAIL resistance by increasing apoptosis in colorectal cancer models. We determined the sensitivity of 27 human colorectal cancer and 2 non-transformed colon epithelial cell lines to TRAIL treatment. A subset of the cancer cell lines with a range of responses to TRAIL was selected from the panel for treatment with TRAIL combined with the PI3 Kinase/mTOR inhibitor PI-103 or the HSP90 inhibitor 17-AAG (tanespimycin). Two TRAIL-resistant cell lines were selected for in vivo combination studies with TRAIL and 17-AAG. We found that 13 colorectal cancer cell lines and the 2 non-transformed colon epithelial cell lines were resistant to TRAIL. We demonstrated that co-treatment of TRAIL and PI-103 or 17-AAG was synergistic or additive and significantly enhanced apoptosis in colorectal cancer cells. This was associated with decreased expression or activity of survival protein biomarkers such as ERBB2, AKT, IKKα and XIAP. In contrast, the effect of the combination treatments in non-transformed colon cells was minimal. We show here for the first time that co-treatment in vivo with TRAIL and 17-AAG in two TRAIL-resistant human colorectal cancer xenograft models resulted in significantly greater tumor growth inhibition compared to single treatments. We propose that combining TRAIL with PI3 Kinase/mTOR or HSP90 inhibitors has therapeutic potential in the treatment of TRAIL-resistant colorectal cancers.

The Auxin Response Factor Transcription Factor Family in Soybean: Genome-Wide Identification and Expression Analyses During Development and Water Stress

In plants, the auxin response factor (ARF) transcription factors play important roles in regulating diverse biological processes, including development, growth, cell division and responses to environmental stimuli. An exhaustive search of soybean genome revealed 51 GmARFs, many of which were formed by genome duplications. The typical GmARFs (43 members) contain a DNA-binding domain, an ARF domain and an auxin/indole acetic acid (AUX/IAA) dimerization domain, whereas the remaining eight members lack the dimerization domain. Phylogenetic analysis of the ARFs from soybean and Arabidopsis revealed both similarity and divergence between the two ARF families, as well as enabled us to predict the functions of the GmARFs. Using quantitative real-time polymerase chain reaction (qRT-PCR) and available soybean Affymetrix array and Illumina transcriptome sequence data, a comprehensive expression atlas of GmARF genes was obtained in various organs and tissues, providing useful information about their involvement in defining the precise nature of individual tissues. Furthermore, expression profiling using qRT-PCR and microarray data revealed many water stress-responsive GmARFs in soybean, albeit with different patterns depending on types of tissues and/or developmental stages. Our systematic analysis has identified excellent tissue-specific and/or stress-responsive candidate GmARF genes for in-depth in planta functional analyses, which would lead to potential applications in the development of genetically modified soybean cultivars with enhanced drought tolerance.

Protein arginine methylation in hepatic glucose metabolism regulation: Histone or nonhistone? That is the question

As Xu etal. stated,1 the previous study by Krones-Herzig etal. clearly demonstrated the functional significance of protein arginine methyltransferase-4 [PRMT4; also known as coactivator-associated arginine methyltransferase-1 (CARM-1)]-dependent regulation of hepatic glucose production in cultured hepatocytes.2 Specifically, they showed that PRMT4 was recruited to the cyclic adenosine monophosphate (cAMP) response element of promoters of both phosphoenol pyruvate carboxykinase (PEPCK) and glucose 6-phosphatase catalytic subunit (G6Pase), which resulted in the increased methylation of arginine 17 on histone H3 and acetylation of histone H4. These results indicated that cAMP response element-binding protein (CREB) might recruit PRMT4 and other known histone acetyltransferases, such as CREB-binding protein (CBP)/p300, onto the promoters of gluconeogenic genes. Indeed, phosphorylation of serine 133 of CREB by cAMP-dependent protein kinase is a key mechanism for the recruitment of CBP/p300 and subsequent activation of CREB-target gene transcription.3 Although we showed that protein arginine methyltransferase-1 (PRMT1) is critical in activating FoxO1-dependent gluconeogenesis by promoting arginine methylation of FoxO1,4 we failed to detect any PRMT1-dependent increase in arginine methylation of histone H3 or H4, at least using the adenovirus-mediated overexpression system in hepatocytes (data not shown). Indeed, we suspect that FoxO1-dependent transcriptional activation might be quite a bit more complicated, because CBP/p300, a potent histone acetyltransferase that normally activates transcription factors, was shown to be involved in the direct acetylation/inhibition of FoxO1.5 Furthermore, recent studies also indicated that histone deacetylase 3 was recruited onto the FoxO1-binding sites of both PEPCK and G6Pase in primary hepatocytes,6 suggesting that certain regions of gluconeogenic promoters might be potentially hypoacetylated. Currently, we are in the process of generating liver-specific knockout mice for PRMT1 to directly address this issue. Further studies utilizing this mouse model will be helpful to decipher the complex histone codes in the regulation of hepatic gluconeogenic gene expression. Dahee Choi B.S.*, Kyoung-Jin Oh Ph.D.*, Seung-Hoi Koo Ph.D.*, * Division of Biochemistry and Molecular Biology, Department of Molecular Cell Biology and Samsung Biomedical Institute, Sungkyunkwan University School of Medicine, Suwon, Korea.

Re-Envisaging the Eight Developmental Stages of Erik Erikson: The Fibonacci Life-Chart Method (FLCM)

The purpose of this study is to describe the use of Fibonacci numbers to model Erikson’s eight developmental stages and to formulate practical clinical implications. Using a new method, called the Fibonacci Life-Chart Method (FLCM), all prospective dates based on the Fibonacci sequence between January 1, 2000 and December 31, 2100 were identified. This study found the FLCM produced a developmental pattern characterized by eight recognizable stages. This finding constitutes a new classification of Erikson’s eight developmental stages. The present research provides support for Erikson’s epigenetic view of predetermined, sequential stages to human development based on the occurrence of Fibonacci numbers in biological cell division and self-organizing systems. This method may help identify populations at risk for psychological disorder, which would allow early intervention. However, a longitudinal study is required to establish its predictive power.

Spatial structure on ocean-exposed sandy beaches: faunal zonation metrics and their variability

Spatial ecological structure is expected to be amplified at interface regions, such as sandy beaches, which form the globe's largest ecotone between the oceans and the land. Yet, the dynamic and unstable nature of sandy shore habitats, coupled with the great mobility and behav- ioural plasticity of beach species, theoretically counteract the development and maintenance of stable spatial structure, such as faunal zonation across the intertidal. We examined spatial struc- ture across the non-vegetated beach-face, using a large data set (3120 replicate samples distrib- uted across 260 cross-shore transects) of intertidal macrobenthos distribution from eastern Aus- tralia. Most (94%) distribution data of the benthic assemblage contained distinct spatial structure, evident as faunal zonation across the shore from the swash to the dunes. A general model recog- nised a tripartite biological division of the shore, but variability in the number of zones was pro- nounced. This variability implies that designs employing low temporal replication may fail to accurately describe the spatial structure on many ocean-exposed sandy beaches. Overall, our data support the prediction of distinct spatial structure based on the prominent interface traits of beach systems as well as the prediction of heterogeneity in spatial structure based on the mobility of beach species and instability of their habitat.