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The evolution of brain lateralization: a game-theoretical analysis of population structure.

In recent years, it has become apparent that behavioural and brain lateralization at the population level is the rule rather than the exception among vertebrates. The study of these phenomena has so far been the province of neurology and neuropsychology. Here, we show how such research can be integrated with evolutionary biology to understand lateralization more fully. In particular, we address the fact that, within a species, left- and right-type individuals often occur in proportions different from one-half (e.g. hand use in humans). The traditional explanations offered for lateralization of brain function (that it may avoid unnecessary duplication of neural circuitry and reduce interference between functions) cannot account for this fact, because increased individual efficiency is unrelated to the alignment of lateralization at the population level. A further puzzle is that such an alignment may even be disadvantageous, as it makes individual behaviour more predictable to other organisms. Here, we show that alignment of the direction of behavioural asymmetries in a population can arise as an evolutionarily stable strategy when individual asymmetrical organisms must coordinate their behaviour with that of other asymmetrical organisms. Brain and behavioural lateralization, as we know it in humans and other vertebrates, may have evolved under basically 'social' selection pressures.

Animals↗

Regulation of a decapentaplegic midgut enhancer by homeotic proteins.

The clustered homeotic genes encode transcription factors that regulate pattern formation in all animals, conferring cell fates by coordinating the activities of downstream 'target' genes. In the Drosophila midgut, the Ultrabithorax (Ubx) protein activates and the abdominalA (abd-A) protein represses transcription of the decapentaplegic (dpp) gene, which encodes a secreted signalling protein of the TGF beta class. We have identified an 813 bp dpp enhancer which is capable of driving expression of a lacZ gene in a correct pattern in the embryonic midgut. The enhancer is activated ectopically in the visceral mesoderm by ubiquitous expression of Ubx or Antennapedia but not by Sex combs reduced protein. Ectopic expression of abd-A represses the enhancer. Deletion analysis reveals regions required for repression and activation. A 419 bp subfragment of the 813 bp fragment also drives reporter gene expression in an appropriate pattern, albeit more weakly. Evolutionary sequence conservation suggests other factors work with homeotic proteins to regulate dpp. A candidate cofactor, the extradenticle protein, binds to the dpp enhancer in close proximity to homeotic protein binding sites. Mutation of either this site or another conserved motif compromises enhancer function. A 45 bp fragment of DNA from within the enhancer correctly responds to both UBX and ABD-A in a largely tissue-specific manner, thus representing the smallest in vivo homeotic response element (HOMRE) identified to date.

Animals↗

Hormonal regulation and expression of vitellogenin multigene family.

Yolk proteins are the most abundant egg proteins in oviparous animals. They are deposited during oocyte maturation for use after fertilization and are synthesized in the liver or fat body as a common precursor termed vitellogenin. Hybridization with cloned DNA complementary to vitellogenin messenger RNA has revealed a surprisingly high degree of evolutionary conservation of sequence of vitellogenin genes among insects, amphibians and birds. The synthesis of vitellogenin in vertebrates is directly under the control of oestrogen at the level of gene transcription. In the frog, Xenopus, vitellogenin genes occur as a multigene family, four of which are actively expressed and are grouped as A and B genes. This multiplicity offers a useful system for investigating the possible selective hormonal regulation of expression of individual members of multigene families. When X. laevis vitellogenin genes were activated by oestrogen in the liver of whole animals or in cultures of parenchymal cells, the two groups of expressed genes were not induced in an identical manner in cells from male and female animals. The activation of A and B groups of genes was non-coordinate in male hepatocytes and coordinate in female cells. Prior exposure of male hepatocytes to oestradiol in vivo or in culture caused the pattern of expression to shift to that in female cells. Since the X. laevis oocyte itself does not synthesize vitellogenin in response to oestrogen, an attempt was made to activate its dormant vitellogenin genes by transferring oestrogen-binding proteins from the liver. Preliminary results show that the microinjection into the oocyte of a preparation containing liver receptor-hormone complex led to the synthesis of vitellogenin by the oocyte. Extension of these experiments will not only enable a more precise analysis of the activation of the vitellogenin multigene family to be made but will also provide direct functional evidence for the role played by steroid hormone receptors in regulating gene expression.

Animals↗

Macro-evolution of the hairy enhancer in Drosophila species.

It has been suggested that many of the changes in the developmental program might be in the cis-acting promoters and enhancer regions. Here I study the macro-evolutionary changes of an enhancer region for the early developmental gene hairy in Drosophila melanogaster, D. simulans, D. pseudoobscura, D. willistoni, D. nebulosa, D. hydei, and D. virilis. The enhancer region is characterized by small, highly conserved blocks interspersed among highly variable regions. Nevertheless, species phylogenies constructed by the enhancer sequences agree with the widely accepted phylogeny of these species. The evolution of the variable regions is consistent with a molecular clock, while the evolution of the conserved blocks is significantly different from a clock. In particular, the D. pseudoobscura lineage shows the highest degree of species-specific change consistent with changes in expression timing reported in an earlier study. It has been suggested that the variation in sequence length between highly conserved blocks may play a role in the coordination of regulatory processes, such as protein-protein interactions; thus, stabilizing selection has been suggested to act on the length variations. Here I develop a test for stabilizing selection on length variation and show that the hairy enhancer does not show statistically significant evidence for stabilizing selection. J. Exp. Zool. (Mol. Dev. Evol.) 291:175-185, 2001.

Amino Acid Sequence↗

Definition of a metal-dependent/Li(+)-inhibited phosphomonoesterase protein family based upon a conserved three-dimensional core structure.

Inositol polyphosphate 1-phosphatase, inositol monophosphate phosphatase, and fructose 1,6-bisphosphatase share a sequence motif, Asp-Pro-(Ile or Leu)-Asp-(Gly or Ser)-(Thr or Ser), that has been shown by crystallographic and mutagenesis studies to bind metal ions and participate in catalysis. We compared the six alpha-carbon coordinates of this motif from the crystal structures of these three phosphatases and found that they are superimposable with rms deviations ranging from 0.27 to 0.60 A. Remarkably, when these proteins were aligned by this motif a common core structure emerged, defined by five alpha-helices and 11 beta-strands comprising 155 residues having rms deviations ranging from 1.48 to 2.66 A. We used the superimposed structures to align the sequences within the common core, and a distant relationship was observed suggesting a common ancestor. The common core was used to align the sequences of several other proteins that share significant similarity to inositol monophosphate phosphatase, including proteins encoded by fungal qa-X and qutG, bacterial suhB and cysQ (identical to amtA), and yeast met22 (identical to hal2). Evolutionary comparison of the core sequences indicate that five distinct branches exist within this family. These proteins share metal-dependent/Li(+)-sensitive phosphomonoesterase activity, and each predicted tree branch exhibits unique substrate specificity. Thus, these proteins define an ancient structurally conserved family involved in diverse metabolic pathways including inositol signaling, gluconeogenesis, sulfate assimilation, and possibly quinone metabolism. Furthermore, we suggest that this protein family identifies candidate enzymes to account for both the therapeutic and toxic actions of Li+ as it is used in patients treated for manic depressive disease.

Amino Acid Sequence↗

Phylogenetic Constraints and Environmental Filtering Jointly Drive Adaptive Evolution in Phragmites australis: From Genetic Structure to Trait Decoupling on the Mongolian Plateau.

The Mongolian Plateau, a typical arid and semi-arid zone in Eurasia, is characterized by highly heterogeneous and fragmented wetland habitats. Phragmites australis, a common wetland species in this region, exhibits remarkable adaptability. Unraveling the coordination between phylogenetic history and local environmental filtering is crucial for elucidating its adaptive mechanisms. Integrating landscape genomics and trait-based phylogenetic analyses, we analyzed transcriptome-wide SNPs, multidimensional functional traits, and environmental variables across 90 individuals from 30 natural P. australis populations. This study aims to reveal the genetic and phenotypic variation patterns underlying population genetic structure and trait variation, specifically distinguishing the roles of geographic isolation, environmental filtering, and phylogenetic history. Results reveal a significant drainage-dependent pattern in genetic structure. Populations in hydrologically connected basins show extensive admixture, whereas those in isolated endorheic basins form distinct lineages. While geographic isolation underpins genetic differentiation, environmental filtering independently explains ~33.84% of the genetic variation, driven primarily by moisture heterogeneity (precipitation seasonality and soil moisture). Crucially, we observed differentiated evolutionary trajectories across functional traits. Structural traits (e.g., plant height, leaf thickness) are phylogenetically conserved; in contrast, physiological traits (e.g., water use efficiency) are decoupled from phylogeny, showing patterns consistent with high plasticity regulated by local environments. This evolutionary decoupling strategy enables P. australis to flexibly adapt to heterogeneous habitats while maintaining structural stability. This study uncovers the synergistic mechanisms by which geographic isolation and environmental filtering jointly shape the genetic patterns of this cosmopolitan species at a regional scale, clarifies that its evolutionary responses may depend heavily on the differentiated plasticity of trait types, and provides valuable regional insights into how widespread wetland species adapt to heterogeneous environments under global change.

Mongolia Plateau↗

Directional selection has shaped the oral jaws of Lake Malawi cichlid fishes.

East African cichlid fishes represent one of the most striking examples of rapid and convergent evolutionary radiation among vertebrates. Models of ecological speciation would suggest that functional divergence in feeding morphology has contributed to the origin and maintenance of cichlid species diversity. However, definitive evidence for the action of natural selection has been missing. Here we use quantitative genetics to identify regions of the cichlid genome responsible for functionally important shape differences in the oral jaw apparatus. The consistent direction of effects for individual quantitative trait loci suggest that cichlid jaws and teeth evolved in response to strong, divergent selection. Moreover, several chromosomal regions contain a disproportionate number of quantitative trait loci, indicating a prominent role for pleiotropy or genetic linkage in the divergence of this character complex. Of particular interest are genomic intervals with concerted effects on both the length and height of the lower jaw. Coordinated changes in this area of the oral jaw apparatus are predicted to have direct consequences for the speed and strength of jaw movement. Taken together, our results imply that the rapid and replicative nature of cichlid trophic evolution is the result of directional selection on chromosomal packages that encode functionally linked aspects of the craniofacial skeleton.

Animals↗

[Anti-infective defence strategies and methods of escape from entomologic pathogens under immunologic control of insects].

Insect immunity comprises a complex of several distinct systems, both haemocytic and humoral in nature, that cooperate together in a more or less coordinated way to provide protection of the body cavity from invading microorganisms. Insects can respond to infections by a selective synthesis of haemolymph immune proteins that are responsible for antibacterial immunity. Antibacterial activity of insect blood is attributable to innate compounds such as lysozome, and to induced polypeptides or small basic proteins absent in non-immunized insects. The cecropins and attacins in Lepidoptera, and diptericins in Diptera are the inducible antibacterial immune proteins well defined biochemically. Bacterial pathogens and some parasites of insects, preferably entomogenous rhabditid nematodes, have developed the mechanism by which they may counteract insect immunity. This phenomenon is realized either by escaping immune reactions or by degrading antimicrobial factors of haemolymph in an active process. Passive resistance of parasites to insect immunity is a result of a strong evolutionary pressure on parasites to develop mechanisms to escape insect immune reactions or to minimize their effectiveness through changes in the parasite itself. Active resistance to the insect non-self response system involves a partial or total destruction of immune proteins by extracellular proteinases released during parasitism.

Animals↗

Evolutionary Process Underlying Receptor Gene Expansion and Cellular Divergence of Olfactory Sensory Neurons in Honeybees.

Olfaction is crucial for animals' survival and adaptation. Unlike the strict singular expression of odorant receptor (OR) genes in vertebrate olfactory sensory neurons (OSNs), insects exhibit complex OR gene expression patterns. In honeybees (Apis mellifera), a significant expansion of OR genes implies a selection preference for the olfactory demands of social insects. However, the mechanisms underlying receptor expression specificity and their contribution to OSN divergence remain unclear. In this study, we used single-nucleus multiomics profiling to investigate the transcriptional regulation of OR genes and the cellular identity of OSNs in A. mellifera. We identified three distinct OR expression patterns, singular OR expression, co-expression of multiple OR genes with a single active promoter, and co-expression of multiple OR genes with multiple active promoters. Notably, ∼50% of OSNs co-expressed multiple OR genes, driven by polycistronic transcription of tandemly duplicated OR genes via a single active promoter. In these OSNs, their identity was determined by the first transcribed receptor. The divergent activation of the promoter for duplicated OR genes ensures the coordinated increased divergence of OSN population. By integrating multiomics data with genomic architecture, we illustrate how fundamental genetic mechanisms drive OR gene expansion and influence flanking regulatory elements, ultimately contributing to the cellular divergence of OSNs. Our findings highlight the interplay between gene duplication and regulatory evolution in shaping OSN diversity, providing new insights into the evolution and adaptation of olfaction in social insects. This study also sheds light on how genetic innovations contribute to the evolution of complex traits.

Animals↗

Fructose-2,6-bisphosphate in control of hepatic gluconeogenesis. From metabolites to molecular genetics.

Hormonal regulation of hepatic gluconeogenic pathway flux is brought about by phosphorylation/dephosphorylation and control of gene expression of several key regulatory enzymes. Regulation by cAMP-dependent phosphorylation occurs at the level of pyruvate kinase and 6-phosphofructo-2-kinase (6PF-1-K)/fructose-2,6-bisphosphatase (Fru-2,6-P2ase). The latter is a unique bifunctional enzyme that catalyzes both the synthesis and degradation of fructose-2,6-bisphosphate (Fru-2,6-P2), which is an activator of 6PF-1-K and an inhibitor of Fru-1,6-P2ase. The bifunctional enzyme is a homodimer whose activities are regulated by cAMP-dependent protein kinase-catalyzed phosphorylation at a single NH2-terminal seryl residue/subunit, which results in activation of the Fru-2,6-P2ase and inhibition of the PF-1-K reactions. Hormone-mediated changes in the phosphorylation state of the bifunctional enzyme are responsible for acute regulation of Fru-2,6-P2 levels. 6PF-2-K/Fru-2,6-P2ase thus provides a switching mechanism between glycolysis and gluconeogenesis in mammalian liver. Pyruvate kinase is regulated by both phosphorylation and allosteric effectors. Fru-1,6-P2, an allosteric activator, also inhibits cAMP-dependent enzyme phosphorylation, and its steady-state concentration is indirectly determined by the level of Fru-2,6-P2. Therefore, acute regulation of both pyruvate kinase and the bifunctional enzyme provide coordinated control at both the pyruvate/phosphoenolpyruvate and Fru-6-P/Fru-1,6-P2 substrate cycles. The Fru-2,6-P2 system is also subject to complex multihormonal long-term control through regulation of 6 PF-2-K/Fru-2,6-P2ase gene expression. Glucocorticoids are the major factor in turning on this gene in liver, but insulin is also a positive effector. cAMP prevents the effects of glucocorticoids and insulin. Although Fru-2,6-P2 plays a key role in the regulation of carbon flux in the gluconeogenic pathway, the regulation of this flux depends on several factors and regulation of other key enzymes whose importance varies depending on the dietary and hormonal status of the animal. Molecular cloning of the cDNA encoding PF-2-K/Fru-2,6-P2ase has elucidated its structure and permitted analysis of its evolutionary origin as well as its tissue distribution and control of its gene expression. The rat liver and skeletal muscle isoforms arose by alternative splicing of a single gene. The muscle form differs from the liver form only at the NH2-terminal and does not have a cAMP-dependent protein kinase phosphorylation site. The hepatic enzyme subunit consists of 470 amino acids.(ABSTRACT TRUNCATED AT 400 WORDS)

Amino Acid Sequence↗

Childhood precursors of psychosis as clues to its evolutionary origins.

Those who as adults will be admitted to a psychiatric ward with a psychotic illness can be distinguished (on the basis of group differences) from others by their behaviour and academic performance at the ages of 7 and 11 years. Pre-schizophrenic boys are anxious and hostile towards adults and peers at the age of 7 years and show poor concentration. By age 11 years these boys are also rated as depressed, and pre-schizophrenic girls as depressed and withdrawn. Pre-affective psychotic boys show minor changes (for example an increase in hostility and restlessness) at age 7 years, although these features are not obvious at age 11 years. Abnormalities that in some respects resemble those in pre-schizophrenic boys are present at age 11 years in a group of females who will be admitted to psychiatric units with non-psychotic diagnoses by the age of 28 years. Academic impairments (including speech and reading difficulties) at ages 7, 11 and 16 years are more severe in pre-schizophrenics than in the other groups. Schizophrenics-to-be are slow to develop continence and show poor coordination and vision at age 7 years, and are rated clumsy at age 16 years. Psychosis reflects a disturbance of aspects of central nervous system function that are time-dependent and in certain respects gender specific. It is argued that the psychoses represent extremes of variation in a gene (or genes) that differs between sexes and controls the timing of development of the two cerebral hemispheres.(ABSTRACT TRUNCATED AT 250 WORDS)

Achievement↗

The evolution of ADHD: a disorder of communication?

Attention deficit hyperactivity disorder (ADHD) is the most commonly diagnosed psychiatric condition. Many believe that the central disability is impaired inhibition, which leads to reduced abilities in social skills, self-control, organization and time management. The behaviors identified by clinicians as problematic--inattention, hyperactivity and impulsivity--have been incorporated into several evolutionary models as selectively adaptive cognitive skills for surviving the challenges of a variable Pleistocene environment. We propose that the "disabilities" exhibited by individuals with ADHD are maladaptive, and we concur with Barkley that there is a central impairment in the behavioral inhibition system. The underlying neural anatomy and physiology support the possibility that neurotransmitter pathology may have an impact on other interlinked systems (including language), and may also account for the frequent comorbidity of aggression, anxiety, depression, and learning disabilities (many of which are language-related). Language skills compete with other cognitive activities for the attentional system, and thus the evolution of language could not in fact be independent of the evolution of attention. If language represents the ultimate expression of the attentional system, and some individuals with ADHD are seriously impaired in the coordination of interlinked neural systems (including language), then ADHD fits Jerome Wakefield's definition of "harmful dysfunction," and communication impairments should be investigated more thoroughly by clinicians.

Adaptation, Physiological↗

Computational identification, cloning, and characterization of IL-1R9, a novel interleukin-1 receptor-like gene encoded over an unusually large interval of human chromosome Xq22.2-q22.3.

The Interleukin-1 receptor (IL-1R) and Toll signaling pathways share the evolutionarily conserved Toll homology domain (THD), which is a critical component in the signaling cascade of the host defense responses to infection and inflammation. Our initial genomic database searches uncovered a novel THD signature sequence between DNA markers DXS87 and DXS366. The feasibility of subsequently applying a coordinated computational approach, including various exon-finding programs, homology-based searches, and receptor profile searches, in revealing the exons encoding this novel IL-1R family member is described. IL-1R9 shows restricted expression in fetal brain and is highly homologous to IL1RAPL (A. Carrie et al., 1999 Nat. Genet. 23: 25-31), which is reportedly involved in nonsyndromic X-linked mental retardation. These genes are scattered over separate genomic intervals in excess of 1.0 Mb and encode receptors with extended C-terminal tails. In our functional NF-kappaB reporter assays, IL1RAPL, IL-1R9, or versions lacking the extended C-terminal sequences failed in responding either to IL-1 directly or to IL-18 when various permutations of IL-18R ectodomain chimeras were fused to their cytoplasmic domains. Evolutionary sequence analyses reinforce our conclusion that these novel orphan receptors probably form a functionally distinct subset of the IL-1R superfamily.

Amino Acid Motifs↗

Evolution of EF-hand calcium-modulated proteins. II. Domains of several subfamilies have diverse evolutionary histories.

In the first report in this series we described the relationships and evolution of 152 individual proteins of the EF-hand subfamilies. Here we add 66 additional proteins and define eight (CDC, TPNV, CLNB, LPS, DGK, 1F8, VIS, TCBP) new subfamilies and seven (CAL, SQUD, CDPK, EFH5, TPP, LAV, CRGP) new unique proteins, which we assume represent new subfamilies. The main focus of this study is the classification of individual EF-hand domains. Five subfamilies--calmodulin, troponin C, essential light chain, regulatory light chain, CDC31/caltractin--and three uniques--call, squidulin, and calcium-dependent protein kinase--are congruent in that all evolved from a common four-domain precursor. In contrast calpain and sarcoplasmic calcium-binding protein (SARC) each evolved from its own one-domain precursor. The remaining 19 subfamilies and uniques appear to have evolved by translocation and splicing of genes encoding the EF-hand domains that were precursors to the congruent eight and to calpain and to SARC. The rates of evolution of the EF-hand domains are slower following formation of the subfamilies and establishment of their functions. Subfamilies are not readily classified by patterns of calcium coordination, interdomain linker stability, and glycine and proline distribution. There are many homoplasies indicating that similar variants of the EF-hand evolved by independent pathways.

Amino Acid Sequence↗

Regulation of early events in chromosome replication.

Eukaryotic genomes are replicated from large numbers of replication origins distributed on multiple chromosomes. The activity of these origins must be coordinated so that the entire genome is efficiently and accurately replicated yet no region of the genome is ever replicated more than once. The past decade has seen significant advances in understanding how the initiation of DNA replication is regulated by key cell-cycle regulators, including the cyclin dependent kinases (CDKs) and the anaphase promoting complex/cyclosome (APC/C). The assembly of essential prereplicative complexes (pre-RCs) at origins only occurs when CDK activity is low and APC/C activity is high. Origin firing, however, can only occur when the APC/C is inactivated and CDKs become active. This two step mechanism ensures that no origin can fire more than once in a cell cycle. In all eukaryotes tested, CDKs can contribute to the inhibition of pre-RC assembly. This inhibition is characterised both by high degrees of redundancy and evolutionary plasticity. Geminin plays a crucial role in inhibiting licensing in metazoans and, like cyclins, is inactivated by the APC/C. Strategies involved in preventing re-replication in different organisms will be discussed.

Anaphase-Promoting Complex-Cyclosome↗

Ovarian expression and function of neuropeptide systems in teleosts and anurans.

The hypothalamic-pituitary-gonadal axis regulates reproduction, sexual maturation, and spawning behaviours. Its evolutionary origins trace back to primitive jawless fish and has been well characterized in teleosts. Recent advances in multi-species genome sequencing, annotation, and experimental approaches for identifying and characterizing key regulators have advanced understanding of neuroendocrine regulation in teleost reproduction, reshaping existing models. Early studies in amphibians established that steroids are critical regulators of final oocyte maturation. Subsequent work in anurans revealed complex interactions among theca cells, follicular cells, and oocytes, supporting a three-cell model in which oocytes contribute to their own steroidogenic environment, challenging the traditional two-cell view of ovarian steroidogenesis. In teleosts, however, direct evidence that oocytes support steroid precursor delivery to theca and follicular cells is limited, and whether a comparable three-cell model applies remains an open hypothesis. Across both taxa, the roles of locally produced neuropeptides in coordinating interactions among theca cells, follicular cells, and oocytes remain largely uncharacterized. Here, we provide a short review of the localization and potential autocrine/paracrine functions of neuropeptides in teleost and amphibian ovaries and discuss existing knowledge gaps. We identify opportunities to leverage detailed localization studies that map neuropeptides to specific ovarian cell types and developmental stages, and discuss how integrating traditional and emerging experimental approaches can advance comparative studies in ovarian endocrinology. This work will improve our understanding of reproductive regulation in fishes and frogs, with applications in captive breeding, aquaculture, and endocrine disruption research.

Autocrine↗

A comparison study of the vertical bias of pyramidal cells in the hippocampus and neocortex.

In this study, we employed morphometric image analysis of the hippocampus proper and temporal lobe neocortex in postmortem tissue to determine vertical bias quantified as Deltatheta, angular dispersion, as well asan index of alignment of cellular elements relative to the radial plane. The radial alignment of cellular elements was consistent with a minicolumnar organization of the cortex. Photomicrographs were taken of the left-hemisphere hippocampal CA3/1 subfields of 13 fetal subjects ranging in gestational age from 19 weeks to 36 weeks and 19 normal individuals aged 4 months to 98 years. For comparison, micrographs from the temporal lobe (Brodmann areas 21 and 22) were similarly processed for layers III and V, where the x-axes of the transformed coordinate system were taken to be the layer III/IV and IV/V borders, respectively. Computerized image analysis measurements of the angular dispersion for the temporal lobe region and hippocampus proper differed significantly within the same brains (p < 0.001). The neocortical layer III exhibited the highest values for Deltatheta, indicating a high degree of columnar organization. Values for Deltatheta in the hippocampal CA subfields were lower but demonstrated significance for the radial alignment of neurons in this area. Values for Deltathetain layer V were intermediate between those of layer III and the hippocampus, consistent with increasing degrees of radial columnar organization of infragranular layers of the neocortex in comparison with the hippocampus and of supragranular in comparison with infragranular neocortical layers. Pyramidal cell arrays within allocortical areas and the neocortex constitute different modular arrangements. This morphological variability may be the expression of evolutionary differences in cortical development.

Adolescent↗

Comparative analysis of cytokinesis in budding yeast, fission yeast and animal cells.

Cytokinesis is a temporally and spatially regulated process through which the cellular constituents of the mother cell are partitioned into two daughter cells, permitting an increase in cell number. When cytokinesis occurs in a polarized cell it can create daughters with distinct fates. In eukaryotes, cytokinesis is carried out by the coordinated action of a cortical actomyosin contractile ring and targeted membrane deposition. Recent use of model organisms with facile genetics and improved light-microscopy methods has led to the identification and functional characterization of many proteins involved in cytokinesis. To date, this analysis indicates that some of the basic components involved in cytokinesis are conserved from yeast to humans, although their organization into functional machinery that drives cytokinesis and the associated regulatory mechanisms bear species-specific features. Here, we briefly review the current status of knowledge of cytokinesis in the budding yeast Saccharomyces cerevisiae, the fission yeast Schizosaccharomyces pombe and animal cells, in an attempt to highlight both the common and the unique features. Although these organisms diverged from a common ancestor about a billion years ago, there are eukaryotes that are far more divergent. To evaluate the overall evolutionary conservation of cytokinesis, it will be necessary to include representatives of these divergent branches. Nevertheless, the three species discussed here provide substantial mechanistic diversity.

Animals↗