Number Of Cortical Cells Research Articles

Pax6 controls cerebral cortical cell number by regulating exit from the cell cycle and specifies cortical cell identity by a cell autonomous mechanism

Many cerebral cortical neurons and glia are produced by apical progenitors dividing at the ventricular surface of the embryonic dorsal telencephalon. Other neurons are produced by basal progenitor cells, which are derived from apical progenitors, dividing away from the ventricular surface. The transcription factor Pax6 is expressed in apical progenitors and is downregulated in basal progenitors, which upregulate the transcription factor Tbr2. Here we show that Pax6−/− cells are under-represented in the cortex of Pax6+/+↔Pax6−/− chimeras early in corticogenesis, indicating that Pax6 is required for the production of normal numbers of cortical cells. We provide evidence that this underproduction is attributable to an early depletion of the progenitor pool caused by greater than normal proportions of newly divided cells exiting the cell cycle. We show that most progenitor cells dividing away from the ventricular surface in Pax6−/− embryos fail to express the transcription factor Tbr2 and that Pax6 is required cell autonomously for Tbr2 expression in the developing cortex of Pax6+/+↔Pax6−/− chimeras. Transcription factors normally expressed ventrally in the telencephalic ganglionic eminences (Mash1, Dlx2 and Gsh2) are upregulated cell autonomously in mutant cells in the developing cortex of Pax6+/+↔Pax6−/− chimeras; Nkx2.1, which is expressed only in the medial ganglionic eminence, is not. These data indicate that early functions of Pax6 in developing cortical cells are to repress expression of transcription factors normally found in the lateral ganglionic eminence, to prevent precocious differentiation and depletion of the progenitor pool, and to induce normal development of cortical basal progenitor cells.

Dopamine manipulation alters immediate-early gene response of striatal parvalbumin interneurons to cortical stimulation

Cortical projections provide the major excitatory inputs to the striatum. In addition to innervating medium spiny cells, these axons contact striatal interneurons that are parvalbumin-immunoreactive (PV-ir). PV-ir interneurons make synaptic connections with many medium spiny cells, and thus can modulate striatal output. The striatum also receives dopaminergic projections from the substantia nigra, but it has been challenging to study the impact of dopamine (DA) cell injury on corticostriatal activity in vivo due to limitations in the methods used to induce cortical activity. Using epidural application of the GABA A antagonist picrotoxin, which produces a topographically restricted region of striatal immediate-early gene expression, we have investigated the effect of DA cell injury or DA receptor antagonism on immediate-early gene (IEG) expression in striatal medium spiny cells and PV-ir interneurons. Epidural application of picrotoxin to the rat's M1 motor cortex induced Fos in ipsilateral dorsolateral striatum. Animals previously given 6-hydroxydopamine (6-OHDA) injections into the ascending DA pathways had greater total numbers of cortical stimulation-induced striatal Fos-ir cells but fewer Fos-ir/PV-ir cells, compared to sham-operates. In a separate experiment, rats given cortical stimulation and treated with the DA D 2-class antagonist eticlopride (0.10 mg/kg) exhibited fewer Fos-ir/PV-ir cells than did vehicle-treated rats. Taken together, these results indicate that DA may importantly control striatal output via influences on PV-ir interneurons. Possible mechanisms for these influences are discussed.

Sex-specific alterations of cerebral cortical cell size in rats exposed prenatally to dioxin

Sex-specific patterns of cerebral cortical lateralization have been documented consistently in both the human and animal brain. Male rats tend to exhibit pronounced right hemisphere dominance compared with females, while females typically exhibit more diffuse lateralization patterns and greater left hemisphere bias compared with males. Prenatal TCDD (2,3,7,8 tetrachlorodibenzo-p-dioxin) exposure produces demasculinization of male offspring sexual behavior, suggesting interference with sexual differentiation of the brain. In previous studies, a reversal of cortical thickness patterns in rats was shown after prenatal TCDD exposure on gestational day 8 (GD 8). The current study, based on the same brain sections, attempted to define changes in the number of cortical cells and cell size distributions in brains of offspring from TCDD-treated dams. Pregnant females were given a single oral dose of 0 or 180 ng kg(-1) TCDD on GD 8. Cell counts and sizes were determined in 3-month-old offspring. Areas 17 and 18a at bregma -3.8 were analysed using digitized, enhanced images of brain sections produced by a photomicroscope fitted with a high-resolution digital camera. Prenatal TCDD exposure altered the relative proportions of smaller and larger cell sizes in male, but not in female offspring. Both exposed males and females, however, exhibited a significant reversal of hemispheric dominance based on cell number. These findings demonstrate that prenatal exposure to TCDD alters the normal patterns of cortical cell asymmetry in a manner consistent with our previous data on thickness patterns.

Ethylene and phosphorus availability have interacting yet distinct effects on root hair development.

The hypothesis that ethylene participates in the regulation of root hair development by phosphorus availability in Arabidopsis thaliana was tested by chemically manipulating ethylene synthesis and response and with ethylene-insensitive mutants. Low phosphorus-induced root hair development could be mimicked by adding the ethylene precursor, 1-aminocyclopropane-1-carboxylate (ACC), to high phosphorus media, and inhibited by adding ethylene inhibitors to low phosphorus media. Ethylene-insensitive mutants showed a reduced response to low phosphorus, indicating ethylene involvement in root hair responses to phosphorus deficiency. To dissect the nature of this involvement, the morphological and anatomical changes associated with increased root hair density were investigated. Growth in low phosphorus resulted in smaller, more numerous cortical cells, resulting in a larger number of root hair-bearing epidermal cell files. Cortical cell number was not affected by ethylene inhibitors, ACC, or mutations reducing ethylene sensitivity in roots grown with low phosphorus, indicating that ethylene does not participate in this response. The exception was the eir1 mutation, which strongly reduced this change in radial anatomy, supporting a role for polar auxin transport in this process. Trichoblast cell length was reduced by low phosphorus availability in all genotypes, but even more so for ein2-1 and ein4. The proportion of epidermal cells forming hairs and root hair length were reduced in ethylene-insensitive mutants, especially in the presence of low phosphorus. These results demonstrate multiple effects of low phosphorus from the earliest stages of root hair development, and cross-talk between ethylene and phosphorus in the control of a subset of the low phosphorus effects, concentrating on those later in development.

Nicotine Abolishes the Hypoxic Induction of Vegf in Human Microvascular Endothelial Cells

Primary microcephaly (OMlM 251200) is an autosomal recessive neurodevelopmental condition in which there is a global reduction in cerebral cortex volume to a size comparable with that of early hominids. This marked reduction in human brain size (e.g. 430g compared with 1450g in the normal adult) raises the question as to whether genes mutated in microcephaly may provide insights into the mechanisms by which brain size has dramatically increased during evolution. We have identified a gene encoding a BRCAl C-terminal domaincontaining protein, mutated in MCPHl families sharing an ancestral 8p23 haplotype. This gene, microcepkalin, is expressed in the developing cerebral cortex of the fetal brain. Sequence homologies suggest a role in DNA repair or cell cycle regulation. The microceplialin gene has been present throughout vertebrate evolution, and we have characterised fish, rodent and primate orthologs. All contain the angiopoeifin-2 gene on the reverse strand in intron 12 of microcephalin. Protein sequence homology is strikingly low, with 57% sequence identity between mouse and human orthologs (c.f. mean human-mouse protein sequence identity, 85%; angiopoeitin-2, 88%). This suggests the potential for significant functional changes during recent evolution. Further studies of microcephalin in different species should provide insights into the regulation of cortical neural cell number, potentially aid understanding of neural progenitor/stem cell regulation and shed light on the evolution of the cerebral cortex.

Expression of Transcriptional Factors of GATA4, GATA6 and SF-1 in the Developmental Process of Rat Adrenal Cortex; The Possible Contribution of GATA4 in Limited Expression before Zonal Establishment.

The adrenal cortex consists of three zones producing different hormones: zona glomerulosa (zG), zona fasciculata (zF) and zona reticularis (zR). Accumulated knowledge has revealed the contribution of transcriptional factors to the functional development of the adrenal cortex, however, the regulatory mechanisms have not yet been fully understood. We studied the expression and localization of transcriptional factors, SF-1, GATA4 and GATA6 by immunohisto-chemistry in the developmental process, establishing three zones of the rat adrenal cortex. The development of the adrenal cortex was monitored by the expression of cortical enzymes, P45011β, P450aldo, and P450scc on gestational days 15, 16, 18, 19, 20 (G15, G16, G18, G19, G20) and postnatal days 1, 2, 20 (P1, P2, P20) in Spraque-Dawley rats. GATA4 expression was observed in a limited number of cortical cells from early gestation (G15) to the neonatal period (P20) before complete establishment of the cortical zones. Nearing the final phase of zG establishment (P20), GATA4 changed its intracellular localization from the nuclei to the perinuclear region. Another noteworthy finding is that GATA6 translocated from the cytoplasm into the nuclei on G19, followed by a leaning distribution of SF-1 in zG (P1) and changing the distribution of SF-1 from zG to zF parallel to the establishment of zG (P20). In conclusion, we report that GATA4 was detected in the immature phase of the adrenal cortex in limited expression but diminished in the mature adrenal cortex. GATA4 may participate in the gene transcription required for the development of the adrenal cortex.

Mental stimulation increases circulating CD4-positive T lymphocytes: a preliminary study

To stimulate the dorsolateral frontal cortex, 12 healthy, adult, human females played contract bridge for 1.5 h between initial and final blood sample collections. Flow cytometric analyses of samples, performed in triplicate, showed a significant increase in CD4-positive T lymphocytes. The dorsolateral frontal cortical thickness is significantly and bilaterally reduced in immune-incompetent female, nude mice. Thymic transplants reverse the deficient cortical thickness and CD4-positive cell numbers.

Viability of dielectrophoretically trapped neural cortical cells in culture

Negative dielectrophoretic trapping of neural cells is an efficient way to position neural cells on the electrode sites of planar micro-electrode arrays. The preservation of viability of the neural cells is essential for this approach. This study investigates the viability of postnatal cortical rat cells that were dielectrophoretically trapped. Morphological characteristics as well as the ratio of the number of outgrowing to the number of non-outgrowing cortical cells were used to compare the viability of trapped cells to that of non-exposed cells. The morphological characteristics include the area of the cell, representing adhesive properties, and the number and length of the processes, as a measure for functional recovery. The results presented in this paper show that the viable state of dielectrophoretically trapped postnatal cortical rat cells under the conditions used was similar to that of non-exposed cells.

Cytological Analysis of Defense-Related Mechanisms Induced in Pea Root Tissues in Response to Colonization by Nonpathogenic Fusarium oxysporum Fo47

The ability of nonpathogenic Fusarium oxysporum, strain Fo47, to trigger plant defense reactions was investigated using Ri T-DNA-transformed pea roots. Cytological investigations of strain Fo47-inoculated roots showed that the fungus grew actively at the root surface and colonized a number of epidermal and cortical cells, inducing marked host cell metabolic changes. In roots inoculated with pathogenic F. oxysporum f. sp. pisi, the pathogen multiplied abundantly through much of the tissues, whereas in Fo47-inoculated roots, fungal growth was restricted to the epidermis and the outer cortex. Invading cells of strain Fo47 suffered from serious alterations, a phenomenon that was not observed in control roots in which F. oxysporum f. sp. pisi grew so actively that the vascular stele was invaded within a few days. Strain Fo47 establishment in the root tissues resulted in a massive elaboration of hemispherical wall appositions and in the deposition of an electron-opaque material frequently encircling pathogen hyphae and accumulating in the noninfected xylem vessels. This suggests that the host roots were signaled to defend themselves through the rapid stimulation of a general cascade of nonspecific defense responses. The specific relationship established between strain Fo47 and the root tissues is discussed in relation to other types of plant-fungus interactions, including pathogenic and symbiotic associations.

Regulation of root hair density by phosphorus availability in Arabidopsis thaliana

ABSTRACTWe characterized the response of root hair density to phosphorus (P) availability in Arabidopsis thaliana. Arabidopsis plants were grown aseptically in growth media with varied phosphorus concentrations, ranging from 1 mmol m−3 to 2000 mmol m−3 phosphorus. Root hair density (number of root hairs per mm of root length) was analysed starting at 7 d of growth. Root hair density was highly regulated by phosphorus availability, increasing significantly in roots exposed to low‐phosphorus availability. The initial root hairs produced by the radicle were not sensitive to phosphorus availability, but began to respond after 9 d of growth. Root hair density was about five times greater in low phosphorus (1 mmol m−3) than in high phosphorus (1000 mmol m−3) media. Root hair density decreased logarithmically in response to increasing phosphorus concentrations within that range. Root hair density also increased in response to deficiencies of several other nutrients, but not as strongly as to low phosphorus. Indoleacetic acid (IAA), the auxin transport inhibitor 2‐(p‐chlorophenoxy)‐2‐methylpropionic acid (CMPA), the ethylene precursor 1‐aminocyclopropane‐1‐carboxylic acid (ACC), and the ethylene synthesis inhibitor amino‐oxyacetic acid (AOA) all increased root hair density under high phosphorus but had very little effect under low phosphorus. Low phosphorus significantly changed root anatomy, causing a 9% increase in root diameter, a 31% decrease in the cross‐sectional area of individual trichoblasts, a 40% decrease in the cross‐sectional area of individual atrichoblasts, and 45% more cortical cells in cross‐section. The larger number of cortical cells and smaller epidermal cell size in low phosphorus roots increased the number of trichoblast files from eight to 12. Two‐thirds of increased root hair density in low phosphorus roots was caused by increased likelihood of trichoblasts to form hairs, and 33% of the increase was accounted for by changes in low phosphorus root anatomy resulting in an increased number of trichoblast files. These results show that phosphorus availability can fundamentally alter root anatomy, leading to changes in root hair density, which are presumably important for phosphorus acquisition.

Pre-inoculation of Ri T-DNA transformed cucumber roots with the mycoparasite, Verticillium lecanii, induces host defense reactions against Pythium ultimum infection

The ability of the mycoparasite, Verticillium lecanii(Zimm.) Vegas, to trigger plant defense reactions was investigated using Ri T-DNA transformed cucumber roots subsequently infected with the root pathogen,Pythium ultimum . The antagonistic potential of V. lecanii against P. ultimum was determined in dual culture tests. Cytological investigations of V. lecanii -inoculated cucumber roots revealed that the fungus grew actively at the root surface and colonized a small number of epidermal and cortical cells, without inducing extensive host cell damage. Direct cell wall penetration was seldom observed and Verticillium ingress into the root tissues proceeded via an intercellular route. In V. lecanii -free roots, the pathogen multiplied extensively through much of the tissues while inV. lecanii -treated roots, pathogen growth was restricted to the epidermis and the outer cortex. At the root surface,V. lecanii interacted with P. ultimum in a way similar to that observed in vitro. However, a novel finding concerned the structural alteration of P. ultimum hyphae that penetrated the root tissues. This was clearly shown by the frequent occurrence of empty fungal cells in intercellular spaces colonized by V. lecanii. Pythium ingress in the root tissues resulted in the deposition of an electron-opaque material frequently encircling pathogen hyphae and also accumulating in the noninfected xylem vessels, suggesting that the host plant was signalled to defend itself through the stimulation of defense mechanisms. The present observations provide the first convincing evidence that V. lecanii may colonize root cells and trigger plant defense reactions in addition to being an efficient mycoparasite.

Multiple Roles of Bone Morphogenetic Protein Signaling in the Regulation of Cortical Cell Number and Phenotype

Members of the bone morphogenetic protein (BMP) family have been implicated in multiple aspects of neural development in both the CNS and peripheral nervous system. BMP ligands and receptors, as well as the BMP antagonist noggin, are expressed in the developing cerebral cortex, making the BMPs likely candidates for regulating cortical development. To define the role of these factors in the developing cerebral cortex, we examined the effects of BMP2 and BMP4 on cortical cells in vitro. Cells were cultured from embryonic day 13 (E13) and E16 rat cerebral cortex in the absence or presence of different concentrations of fibroblast growth factor 2, a known regulator of cortical cell proliferation and differentiation. At E13, the BMPs promoted cell death and inhibited proliferation of cortical ventricular zone cells, resulting in the generation of fewer neurons and no glia. At E16, the effects of the BMPs were more complex. Concentrations of BMP2 in the range of 1-10 ng/ml promoted neuronal and astroglial differentiation and inhibited oligodendroglial differentiation, whereas 100 ng/ml BMP2 promoted cell death and inhibited proliferation. Addition of the BMP antagonist noggin promoted oligodendrogliogenesis in vitro, demonstrating that endogenous BMP signaling influences the differentiation of cortical cells in vitro. The distribution of BMP2 and noggin within the developing cortex suggests that local concentrations of ligands and antagonists define gradients of BMP signaling during corticogenesis. Together, these results support the hypothesis that the BMPs and their antagonist noggin co-regulate cortical cell fate and morphogenesis.

Loss of Nkx2.1 homeobox gene function results in a ventral to dorsal molecular respecification within the basal telencephalon: evidence for a transformation of the pallidum into the striatum.

The telencephalon is organized into distinct longitudinal domains: the cerebral cortex and the basal ganglia. The basal ganglia primarily consists of a dorsal region (striatum) and a ventral region (pallidum). Within the telencephalon, the anlage of the pallidum expresses the Nkx2.1 homeobox gene. A mouse deficient in Nkx2.1 function does not form pallidal structures, lacks basal forebrain TrkA-positive neurons (probable cholinergic neurons) and has reduced numbers of cortical cells expressing GABA, DLX2 and calbindin that migrate from the pallidum through the striatum and into the cortex. We present evidence that these phenotypes result from a ventral-to-dorsal transformation of the pallidal primordium into a striatal-like anlage.

Fas/Apo [Apoptosis]-1 and Associated Proteins in the Differentiating Cerebral Cortex: Induction of Caspase-Dependent Cell Death and Activation of NF-κB

The developing cerebral cortex undergoes a period of substantial cell death. The present studies examine the role of the suicide receptor Fas/Apo[apoptosis]-1 in cerebral cortical development. Fas mRNA and protein are transiently expressed in subsets of cells within the developing rat cerebral cortex during the peak period of apoptosis. Fas-immunoreactive cells were localized in close proximity to Fas ligand (FasL)-expressing cells. The Fas-associated signaling protein receptor interacting protein (RIP) was expressed by some Fas-expressing cells, whereas Fas-associated death domain (FADD) was undetectable in the early postnatal cerebral cortex. FLICE-inhibitory protein (FLIP), an inhibitor of Fas activation, was also expressed in the postnatal cerebral cortex. Fas expression was more ubiquitous in embryonic cortical neuroblasts in dissociated culture compared to in situ within the developing brain, suggesting that the environmental milieu partly suppresses Fas expression at this developmental stage. Furthermore, FADD, RIP, and FLIP were also expressed by subsets of dissociated cortical neuroblasts in culture. Fas activation by ligand (FasL) or anti-Fas antibody induced caspase-dependent cell death in primary embryonic cortical neuroblast cultures. The activation of Fas was also accompanied by a rapid downregulation of Fas receptor expression, non-cell cycle-related incorporation of nucleic acids and nuclear translocation of the RelA/p65 subunit of the transcription factor NF-kappaB. Together, these data suggest that adult cortical cell number may be established, in part, by an active process of receptor-mediated cell suicide, initiated in situ by killer (FasL-expressing) cells and that Fas may have functions in addition to suicide in the developing brain.

Detection of synaptophysin-producing cells in human thymus by immunohistochemistry and nonradioactive in situ hybridization.

We investigated human thymic tissue by immunohistochemistry and in situ hybridization for the presence of synaptophysin-producing cells. Our results indicate that anti-synaptophysin antibody detected immunoreactive material in nerve fibers around vessels located in major thymic septa, in a relevant number of cortical epithelial cells, and in scattered epithelial cells in the medulla. The epithelial nature of synaptophysin-positive cells was documented by the co-expression of cytokeratins as revealed by double immunofluorescence. In situ hybridization studies revealed the presence of synaptophysin mRNA in cells mainly located in the cortex, the specific fluorescent signals being localized in the cell cytoplasm. Western blot analysis using an affinity-purified polyclonal antibody revealed an immunoreactive band of about 38 kD in the extracts from unfractionated thymic tissue and from epithelial cell-enriched fractions. No staining was observed in isolated thymocytes. The expression of synaptophysin in epithelial cells of the thymic cortex suggests that this protein may be involved in secretory activities related to T-cell maturation.

Cell death in the brain of the HTx rat.

The structural changes in the hydrocephalic brain suggest that cell death must be a significant factor in the loss of cortical mantle thickness and cell numbers. In the developing hydrocephalic brain a similar conclusion might also be reached. We present data suggesting that in the developing hydrocephalic HTx rat brain, there are at least two processes that underlie the structural deficit in the cortex. The first is abnormal development of the cortex probably resulting from a combination of the genetic defect and blockage of CSF circulation in the fetus. The second is a direct consequence of raised intracranial pressure and is manifested in a lack of development of glial cells in the neonatal brain and in the loss of myelination and neurones as pressure rises after birth, particularly after skull plate fusion. We find little evidence of increased cell death by apoptosis, recording instead a decrease in apoptotic index. There is evidence that necrosis must have occurred.

Spatial distribution of chitinases and β‐1,3‐glucanase transcripts in bean arbuscular mycorrhizal roots under low and high soil phosphate conditions

Arbuscular mycorrhizal (AM) fungi extensively colonize the root cortex under low‐soil‐phosphate (P) conditions, whereas infection is limited under high‐P conditions. Fungal growth under both P conditions might be influenced by plant defence‐related gene expression. In this study, we used in situ hybridization methods to compare the cellular localization of three defence‐related mRNAs in non‐infected bean roots and in relation to fungal infection units. In non‐infected and infected roots, mRNAs encoding acidic and basic endochitinases were generally most abundant in the vascular cylinder. High‐P‐grown mycorrhizal roots showed localized accumulation of the acidic endochitinase mRNA in cortical cells containing arbuscules and in their immediate vicinity (one to five cell layers). The pattern of accumulation of the basic endochitinase mRNA was not affected by P or AM fungal infection. At the low P concentration, the β‐1,3‐glucanase mRNA accumulated predominantly in the vascular cylinder of non‐infected roots. Suppression of β‐1,3‐glucanase mRNA accumulation in these tissues was observed in non‐infected roots at the high‐P and in mycorrhizal roots at both P concentrations. The observed suppression extends at least several mm from fungal infection units, characterizing a systemic effect. Beta‐1,3‐glucanase mRNA accumulated also around a number of cortical cells containing arbuscules only at the low P concentration. The localized accumulations of the endochitinase and β‐1,3‐glucanase mRNAs suggest that the encoded proteins might be involved in the control of intraradical fungal growth.

Nonhuman Primate Model of the Effect of Prenatal Cocaine Exposure on Cerebral Cortical Development.

To investigate the effects of prenatal cocaine exposure on the corticogenesis in primates we developed a monkey model in which pregnant animals received 10 mg/kg cocaine orally twice a day from the 40th to the 102nd day of pregnancy. The animals gave birth at term, and brains of the 2-month and 1.5-year-old infants were examined. Examination revealed the structural abnormalities throughout the cerebral cortex that would be expected from modulation of the nonselectively diffusing circulation-derived monoamines. They include: (1) reduction in the number of cortical cells, which most likely reflects abnormal cell proliferation; (2) inappropriate positioning of cortical neurons, which resulted from alterations in migration of cortical cells; and (3) altered glial morphology. The structural alterations were accompanied by abnormalities in animal temperament reminiscent of those seen in human infants of drug-abusing mothers. As predicted by the morphologic studies, we found that cocaine treatment produced significant changes in the levels of monoamines and their receptors in all laminae of the frontal, parietal, temporal, and occipital regions of the fetal cerebral wall. This indicates that cocaine abuse by pregnant human mothers may affect the global levels of monoamines in the fetal brain and, in doing so, interfere with a broad range of developmental events regulated by these chemicals.

Induction of systemic resistance to Pythium damping‐off in cucumber plants by benzothiadiazole: ultrastructure and cytochemistry of the host response

Benzo (1,2,3) thiadiazole-7-carbothioic acid S-methyl ester (BTH, CGA 245704), a non-toxic, synthetic chemical, was applied as a foliar spray to cucumber plants and evaluated for its potential to induce defense mechanisms in root tissues infected by the soilborne pathogen, Pythium ultimum Trow. In non-treated cucumber plants, fungal colonization was intense and paralleled marked host tissue damage, whereas in BTH-treated plants, pathogen ingress towards the vascular stele was apparently halted by the massive deposition of a phenolic-enriched material which occluded a large number of cortical and vascular parenchyma cells. This considerable increase in the accumulation of phenolics was accompanied by cytological disorders of the invading pathogen at a time when the wall-bound cellulose component was preserved. In addition to phenolic compounds, the occluding material contained large amounts of beta-glucoside residues. These residues gradually decreased in the areas neighboring fungal cells whereas phenolic deposition appeared to be more uniformly distributed throughout the occluded host cells. Pathogen penetration in non-occluded cucumber root cells coincided with other changes, mainly characterized by both the deposition onto the inner surface of the cell walls of some heterogeneous wall appositions and the coating of some intercellular spaces with an electron-opaque material. Evidence is provided in this study that BTH has the ability to induce SAR in cucumber. Exogenous, foliar applications of the chemical sensitize susceptible cucumber plants to react more rapidly and more efficiently to P. ultimum attack, mainly through the massive accumulation of phenolic compounds at sites of attempted pathogen penetration.

Changes in cell-cycle kinetics during the development and evolution of primate neocortex.

The evolutionary expansion of neocortical size in mammals is particularly prominent in anthropoid primates (i.e., monkeys, apes, and humans) and reflects an increased number of cortical cells, yet the developmental basis for this increase remains undefined. Cortical cell production depends on the length of the cell-division cycle of progenitor cells during neurogenesis, which previously has been measured only in smaller-brained rodents. To investigate whether cortical expansion in primates reflects modification of cell-cycle kinetics, we determined cell-cycle length during neurogenesis in the proliferative cerebral ventricular zone of fetal rhesus monkeys, by using cumulative S-phase labeling with bromodeoxyuridine. Cell-cycle durations in monkeys were as much as 5 times longer than those reported in rodents. Nonetheless, substantially more total rounds of cell division elapsed during the prolonged neurogenetic period of the monkey cortex, providing a basis for increased cell production. Moreover, unlike the progressive slowing that occurs during cortical development in rodents, cell division accelerated during neurogenesis of the enlarged cortical layers in monkeys. These findings suggest that evolutionary modification of the duration and number of progenitor cell divisions contributed to both the expansion and laminar elaboration of the primate neocortex.