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PubMed2001

ngl9: a third MADS box gene expressed in alfalfa root nodules.

Expression of MADS box genes has previously been localized to the infected cells of alfalfa (Medicago sativa) root nodules. These genes represent the first putative transcription factors to be identified in nodules and are hypothesized to be involved in a signal transduction pathway initiated by the intracellular bacterium. The eventual activation of specific target genes defines pertinent characteristics of this nitrogen-fixing differentiated cell. In this study, we identify a third nodule MADS box gene, ngl9, and demonstrate that the DNA-binding activity of its protein product is dependent on the presence of a second MADS box protein, NMH7. Despite previous results to the contrary, both genes are expressed in the early stages of flower development, further strengthening the premise that nodule developmental programming may capitalize upon existing developmental cascades.

Amino Acid Sequence↗

PubMed2005

A population-based study of the recurrence of developmental disabilities--Metropolitan Atlanta Developmental Disabilities Surveillance Program, 1991-94.

Serious developmental disabilities (DD) are quite common and affect approximately 2% of all school-aged children. The impact of DDs with respect to the need for special education services, medical care and the demand on family members can be enormous. While this impact can be magnified for families with more than one child with a DD, little is known regarding the epidemiology of recurrence of DDs. When the cause of a DD is unknown, genetic counsellors rely on recurrence risk estimates which for DDs are over 10 years old. The objectives of our study were to: (1) assess the contribution of recurrent cases to the prevalence of DDs; (2) provide current, population-based recurrence risk estimates; and (3) examine characteristics of the first affected child as predictors of recurrence. Two population-based data sources were used to identify all children born to the same mother during the period 1981-91 in the five-county metropolitan Atlanta area with at least one of four DDs: mental retardation (MR), cerebral palsy, hearing loss, or vision impairment. Recurrence risk estimates for these DDs ranged from 3% to 7% and were many times higher than the background prevalences. The risk of recurrence of DDs was greatest for MR - approximately eight times greater than the baseline MR prevalence. Isolated mild MR (IQ 50-70) was highly concordant between siblings with MR. Sex, race, and birthweight of the index child, maternal education, and maternal age were not significantly associated with recurrence risk. Further research is needed to investigate the roles of genetic and environmental factors on the recurrence of DDs, particularly isolated mild MR.

Child↗

PubMed1999

Developmental care teams in the neonatal intensive care unit: survey on current status.

Developmental Care Teams (DCT) have evolved in Neonatal Intensive Care Units (NICUs) in response to mounting evidence that developmental care is cost-effective and improves outcomes of critically ill newborns. Lack of national practice guidelines and standardized roles for DCT members prompted formulation and distribution of a questionnaire to obtain information regarding staff membership of DCTs, budgeting for DCTs, utilization of developmental care in practice, and education and developmental training of NICU staff. Questionnaires were sent to 50 NICUs in 30 states, with a return rate of 62% (31 of 50), representing 18 different states. Of those who responded, 64% had a DCT, and an additional 24% were in various phases of starting a team. Forty-three percent of the teams meeting on a regular basis did so monthly. Only 30% of those with a DCT had a dedicated budget to cover operating costs of their developmental program. Fifty-two percent of respondents had Neonatal Individualized Developmental Care and Assessment Program (NIDCAP)-certified staff at their institutions; however, nine other types of developmental specialists were also listed. Only four respondents indicated utilization of set criteria for initiation of a DCT consult, and 74% of those with DCTs initiated consults "when the need arises." NIDCAP assessments were used for parent teaching (54%), care plans (69%), care recommendations (46%), and at caregiver "discretion" (39%). The results of the survey validated an intense interest in developmental care. Approach to developmental care is variable between NICUs and implementation as outlined by NIDCAP is unusual. Practical guidelines for utilization and funding of DCTs are needed.

Child Development↗

PubMed1997

A mutational analysis of conjugation in Tetrahymena thermophila. 1. Phenotypes affecting early development: meiosis to nuclear selection.

Conjugation in the freshwater ciliate Tetrahymena thermophila involves a developmental program that models meiosis, fertilization, and early developmental events characteristic of multicellular eukaryotes. We describe a gallery of five early-acting conjugation mutations. These mutants, cnj1-5, exhibit phenotypes in which specific steps in the conjugal pathway have been altered or eliminated. Specifically, cnj1 and cnj2 fail to condense their micronuclear chromatin prior to each of the three prezygotic nuclear divisions. This results in nuclear division failure, failure to replicate DNA, and failure to initiate postzygotic development. The cnj3 mutant appears to exhibit a defect in chromosome separation during anaphase of mitosis. cnj4 mutants successfully carry out meiosis I, yet are unable to execute the second meiotic division and abort all further development. cnj5 mutants are unable to initiate either meiosis I or meiosis II, yet proceed to execute all subsequent developmental events. These mutant phenotypes are used to draw inferences regarding developmental dependencies that exist within the conjugation program.

Animals↗

PubMed1983

A new method for examining the complexity and relationships of "timers" in developing systems.

Simple methods are developed for analyzing the rate-limiting pathways, or "developmental timers," for consecutive stages in a developing system. Two conditions are first defined for short and long timing to a developmental stage. Shifts are then performed at time intervals from short to long and long to short conditions. The total time to the stage (time under first condition plus time under second condition) is scored and plotted as a function of the time of shift, resulting in two plots, one for shifts from the short to long condition, and the other for shifts from the long to short condition. Each plot is then analyzed for the number of components, slopes of components, absolute times of origins and termini of components, and discontinuities between components. This information is then used (1) to distinguish between single- and multiple-component timers, (2) to assess the sensitivity of each timer component to the change in the environmental condition employed in the method, including reversibility, (3) to test for the addition of a new timer component under long conditions, and (4) to test for an identity change of a timer component between short and long conditions. These interpretations in turn provide a minimum estimate of the complexity of the rate-limiting pathway to a developmental stage, temporally define major transition points between timer components, and provide some insight into the nature of timer components. By characterizing the rate-limiting pathway from the origin of a developmental program for each consecutive stage in that program, distinctions can also be made between single, parallel, sequential, and branching timer relationships. From these interpretations, a detailed temporal "map" of the rate-limiting program can be generated for any developmental system in which consecutive stages can be reproducibly monitored with time.

Animals↗

PubMed1997

Gravity, light and plant form.

Plants have evolved highly sensitive and selective mechanisms that detect and respond to various aspects of their environment. As a plant develops, it integrates the environmental information perceived by all of its sensory systems and adapts its growth to the prevailing environmental conditions. Light is of critical importance because plants depend on it for energy and, thus, survival. The quantity, quality and direction of light are perceived by several different photosensory systems that together regulate nearly all stages of plant development, presumably in order to maintain photosynthetic efficiency. Gravity provides an almost constant stimulus that is the source of critical spatial information about its surroundings and provides important cues for orientating plant growth. Gravity plays a particularly important role during the early stages of seedling growth by stimulating a negative gravitropic response in the primary shoot that orientates it towards the source of light, and a positive gravitropic response in the primary root that causes it to grow down into the soil, providing support and nutrient acquisition. Gravity also influences plant form during later stages of development through its effect on lateral organs and supporting structures. Thus, the final form of a plant depends on the cumulative effects of light, gravity and other environmental sensory inputs on endogenous developmental programs. This article is focused on developmental interactions modulated by light and gravity.

Arabidopsis↗

PubMed2002

[Evaluation of the developing human visual system using flash-visual evoked potential].

Flash visual evoked potential (Flash-VEP) is easily recorded in preterm infants. However, its clinical application has not been established due to its great variability in response. Our longitudinal studies on the two components of the N1 wave facilitated peak definition and established normal ranges that are clinically valuable. The N1a (early component of the N1) peak latency decreases at about 4.6 msec/week between 30 and 40 weeks postmenstrual age. A flash-VEP study in the preterm period enables us to observe the neuronal development in the human visual system that normally proceeds in utero. Flash-VEP analyses on preterm infants demonstrated that the decrease in the N1a peak latency reflects the progress of myelination in the visual pathway according to the developmental program irrespective of preterm birth. The developmental changes of the N1 wave configuration reflect the maturation of the neuronal networks in the visual cortex, which is accelerated by extrauterine visual experience. Using improved methodology and peak denomination that we proposed, flash-VEP can be applied to preterm infants safely, and should provide us with neuro-developmental information of the human cerebrum.

Cerebral Hemorrhage↗

PubMed1999

Apoptosis and predisposition to oral cancer.

The term apoptosis, also known as programmed cell death (PCD), was coined by developmental biologists a number of years ago to describe a form of cell death characterized by several unique morphological and biochemical features. Genetic studies of the round worm Caeneorhabditis elegans, a simple multicellular organism, first revealed apoptosis to be an integral part of the developmental program. Subsequently, the importance of apoptosis in higher organisms was demonstrated in several eukaryotic systems. [n mammals, apoptosis is widespread during embryogenesis and in adult tissues. It is required for normal tissue homeostasis and for clonal selection in the immune system. In both developing and adult organisms, apoptosis plays a central role in reinforcing appropriate cellular patterns and in regulating cell number by eliminating cells that are harmful or no longer needed. It is becoming increasingly clear that disruption in the apoptosis pathway can contribute to the development of a number of developmental, inflammatory, degenerative, and neoplastic diseases. The effector arm of the apoptotic program includes members of the Bcl-2 gene family that function as either death agonists or death antagonists. These proteins participate in an elaborate genetically controlled biochemical pathway that functions to maintain tissue and organ homeostasis and serve as a critical defense mechanism to guard against malignant transformation. Cancer is the result of a series of genetic lesions that include activation of oncogenes and inactivation or loss of tumor suppressor genes. Several groups of investigators have observed that deregulated expression of oncogenes can subvert apoptotic pathways, resulting in prolonged cell survival. In pathological settings such as cancer, members of the Bcl-2 gene family are able to synergize with oncogenes and tumor suppressor genes to transform cells. In this review, we describe the process of apoptosis in mammalian cells and define the role and biochemical pathways through which the Bcl-2 gene family induce and/or protect cells from apoptosis. Last, we will discuss the evidence which suggests that alterations in this pathway may play a central role in tumorigenesis by allowing genetically damaged cells normally destined for elimination to persist, predisposing them to additional mutations and driving them to malignancy.

Adult↗

PubMed2004

Embryonic and fetal programming of physiological disorders in adulthood.

In the past decade, data from numerous epidemiological studies have indicated strong inverse associations between birth weight and risk of coronary heart disease, hypertension, type 2-diabetes, and other diseases in adulthood. The "Barker hypothesis" thus postulates that a number of organ structures and functions undergo programming during embryonic and fetal life. This developmental programming determines the set points of physiological and metabolic responses in adult life. Alterations of nutrient availability during gestation may lead to developmental adaptations, via hormonal maneuvers by the embryo and fetus that readjust these set points. These adaptive measures have short-term benefits to the embryo and fetus, so that the newborn will be better prepared for the adverse environment (e.g., undernutrition). However, adequate nutritional support during postnatal life that enables catch-up growth may create metabolic conflicts that predispose the adult to aberrant physiological functions and, ultimately, increased risk of disease. It is plausible that other adverse in utero conditions, including exposure to developmental toxicants, may similarly alter adult disease susceptibility. This article provides an overview of the Barker hypothesis, its supporting evidence, the current advances in understanding the biological mechanisms underlying this phenomenon, and its implications for developmental toxicology.

Animals↗

PubMed2003

Post-transcriptional regulation of the Streptomyces coelicolor stress responsive sigma factor, SigH, involves translational control, proteolytic processing, and an anti-sigma factor homolog.

The sigH gene encodes a sigma factor whose transcription is controlled by stress regulatory systems and the developmental program in Streptomyces coelicolor. Here, we describe developmentally regulated post-transcriptional control systems for SigH. sigH is expressed as three primary translation products, SigH-sigma(37), SigH-sigma(51), and SigH-sigma(52). In vitro, SigH-sigma(52) was comparable to SigH-sigma(37) in its ability to associate with RNA polymerase core enzyme and specifically initiate transcription in vitro. While SigH-sigma(51/52) were the primary gene products observed throughout early phases of growth, their abundance decreased during later stages in liquid or solid phase cultures while levels of shorter, C-terminally encoded products increased. These included SigH-sigma(37), a product of the downstream translational initiation site, as well as two proteolytic derivatives of SigH-sigma(51/52) (34kDa and 38kDa). Accumulation of SigH-sigma(37) and processing of SigH-sigma(51/52) into these stable 34kDa and 38kDa derivatives correlated with morphological changes on solid medium and physiological maturation in liquid medium. SigH-sigma(51/52) processing did not occur on medium non-permissive for aerial mycelium formation or in one particular developmental mutant (brgA). The proteolytic activity could be detected in vitro using crude extracts of stationary phase cultures, but was absent from exponential phase cultures. prsH, the gene upstream of sigH having sequence similarity to known anti-sigma factors, was able to bind to, and thus presumably inactivate SigH-sigma(52), SigH-sigma(51), and SigH-sigma(37). We have shown elsewhere that prsH was conditionally required for colonial development. Thus, while at least one transcriptional regulator is known to bring about the accumulation of sigH mRNA at different times and different locations in colonies, the post-transcriptional processes described here regulate the activity of different SigH isoforms and program their temporal accumulation pattern, i.e. the elimination of SigH-sigma(51/52) and accumulation of SigH-sigma(37)-like proteins, as a function of development.

Amino Acid Sequence↗

PubMed2000

Genotype, phenotype, and developmental biology of molar tooth characters.

Primate molar shapes reflect developmental and ecological processes. Development may constrain as well as facilitate evolution of new tooth shapes, affecting how reliable dental characters are in phylogenetic studies. Much of the genetic machinery of development uses the same genes among different organs, including teeth, limbs, and feathers. Furthermore, within a tooth, the development of individual cusps repeatedly uses the same set of developmental genes, forming a "developmental module." The repeated activation of the developmental module can explain the cumulative variation in later-developing cusps. Therefore short, later-developing cusps may be evolvable but also more homoplastic. This patterning cascade mode of cusp development can be used to explain the variational properties of dental characters and character states related to cusp initiation. The developmental basis and variational properties of crown termination, cusp shape, and cusp configuration characters are currently less well understood. It is unlikely that there is a simple "gene to phenotype" map for dental characters. Rather, the whole cusp pattern is a product of a dynamic developmental program manifested in the activation of the developmental modules.

Animals↗

PubMed1994

Gene expression in single cells of Bacillus subtilis: evidence that a threshold mechanism controls the initiation of sporulation.

Early during endospore formation in the bacterium Bacillus subtilis, two distinct cell types are formed. The initiation of this developmental pathway requires several physiological conditions (e.g., nutrient deprivation) and is controlled by the Spo0A transcription factor. We have found that in a culture of sporulating cells, there are two subpopulations, one that has initiated the developmental program and activated the expression of early developmental genes and one in which early developmental gene expression remains uninduced. We measured the expression of developmental (spo) genes in single cells of B. subtilis by using spo-lacZ fusions. Cells containing a spo-lacZ fusion were stained with a dye that fluoresces upon hydrolysis by beta-galactosidase, and the fluorescence in individual cells was measured with a flow cytometer. For Spo+ cells, we found that the proportion of the population expressing early developmental genes correlates well with the fraction of the population that eventually produces spores. In addition, mutations that cause a decrease in the amount of activated (phosphorylated) Spo0A transcription factor cause a decrease in the size of the subpopulation expressing early developmental genes that are directly activated by Spo0A approximately P. Again, the size of the subpopulation correlates well with the fraction of cells that produce spores. These results indicate that a threshold level of activated Spo0A (Spo0A approximately P) or of a component of the phosphorylation pathway must accumulate to induce sporulation gene expression and that most of the cells that are able to induce the expression of early genes that are directly activated by Spo0A approximately P go on to produce mature spores.(ABSTRACT TRUNCATED AT 250 WORDS)

Bacillus subtilis↗

PubMed1995

Redox regulation of programmed cell death in lymphocytes.

A redox imbalance caused by an over-production of prooxidants or a decrease in antioxidants seems to play a role in the programmed cell death that occurs in various developmental programs. Such a physiological function for oxidative stress is particularly applicable to the immune system, wherein individual lymphocytes undergo continuous scrutiny to determine if they should be preserved or programmed to die. Following activation, lymphocytes produced increased levels of reactive oxygen species (ROS) which may serve as intracellular signaling molecules. The ultimate outcome of this increased ROS formation, i.e., lymphocyte proliferation versus programmed cell death, may be dictated by macrophage-derived costimulatory molecules that bolster or diminish lymphocyte antioxidant defenses. HIV-1-infected individuals display multiple symptoms of redox imbalance consistent with their being in oxidative stress, and lymphocytes from such individuals are more prone to undergo apoptosis in vitro. It is suggested that oxidative stress, and lymphocytes from such individuals are more prone to undergo apoptosis in vitro. It is suggested that oxidative stress is a physiological mediator of programmed cell death in lymphoid cells, and that HIV disease represents an extreme case of what can happen when regulatory safeguards are compromised.

Apoptosis↗

PubMed2006

Aging and immortality: quasi-programmed senescence and its pharmacologic inhibition.

While ruling out programmed aging, evolutionary theory predicts a quasi-program for aging, a continuation of the developmental program that is not turned off, is constantly on, becoming hyper-functional and damaging, causing diseases of aging. Could it be switched off pharmacologically? This would require identification of a molecular target involved in cell senescence, organism aging and diseases of aging. Notably, cell senescence is associated with activation of the TOR (target of rapamycin) nutrient- and mitogen-sensing pathway, which promotes cell growth, even though cell cycle is blocked. Is TOR involved in organism aging? In fact, in yeast (where the cell is the organism), caloric restriction, rapamycin and mutations that inhibit TOR all slow down aging. In animals from worms to mammals caloric restrictions, life-extending agents, and numerous mutations that increase longevity all converge on the TOR pathway. And, in humans, cell hypertrophy, hyper-function and hyperplasia, typically associated with activation of TOR, contribute to diseases of aging. Theoretical and clinical considerations suggest that rapamycin may be effective against atherosclerosis, hypertension and hyper-coagulation (thus, preventing myocardial infarction and stroke), osteoporosis, cancer, autoimmune diseases and arthritis, obesity, diabetes, macula-degeneration, Alzheimer's and Parkinson's diseases. Finally, I discuss that extended life span will reveal new causes for aging (e.g., ROS, 'wear and tear', Hayflick limit, stem cell exhaustion) that play a limited role now, when quasi-programmed senescence kills us first.

Aging↗

PubMed2002

p53 regulates apoptotic retinal ganglion cell death induced by N-methyl-D-aspartate.

PURPOSE: The tumor suppressor protein p53 plays a central role in regulating apoptosis in a variety of neuronal cell types. Previous studies have indicated that retinal ganglion cell (RGC) death induced by ischemia follows a p53-dependent pathway. Ischemia causes wide-spread damage to the retina, eliciting multiple different damaging pathways. We conducted experiments to specifically investigate the role of p53 in RGC death activated by overstimulation of the N-methyl-D-aspartate (NMDA) receptor, an ionotropic glutamate dependent calcium channel normally involved in glutamate neurotransduction. METHODS: RGC death was induced in both wild-type (CB6F1 or 129/Sv) and p53-deficient (129/Sv background) mice by a single intravitreal injection of either 40 or 160 nmol of NMDA into one eye leaving the other eye as an untreated control. Cell loss was quantified by comparing the number of surviving cells in the retinas from experimental eyes relative to the control eyes of the same animals. The accumulation of p53 mRNA in retinas was monitored by reverse-transcription PCR (RT-PCR) of retinal total RNA isolated from mice injected with 40 nmol of NMDA. The functional requirement for p53 was monitored in p53-deficient mice after intravitreal injection of 160 nmol of NMDA. Immunohistochemistry for cleaved poly(ADP-ribose) polymerase (PARP) was performed on p53-deficient mice after intravitreal injection of 160 nmol of NMDA. RESULTS: In wild-type CB6F1 mice, p53 mRNA levels are elevated within 3 h after NMDA injection. This accumulation correlates with the onset of changes in RGC nuclear morphology that precedes pyknosis, which occurs by 6 h. Mice (129/Sv) deficient for one or both alleles of p53 show no developmental change in RGC number, compared to wild-type animals (Mann-Whitney test, p=0.824), suggesting that p53 is not required for developmental programmed cell death of RGCs. In adult mice, however, p53-dependent changes in the rate of RGC death after exposure to 160 nmol of NMDA were observed. Four days after injection, p53+/+ and p53-/- mice exhibit statistically equivalent amounts of cell loss (p>0.1), while p53+/- mice have significantly attenuated cell loss (p<0.002), relative to the other groups. RGCs from NMDA-treated p53+/+ and p53-/- mice were analyzed further using immunohistochemistry to identify the cleavage products of poly(ADP-ribose) polymerase (PARP), a known substrate for caspases. Cleaved PARP was found in p53+/+ and p53+/- eyes, but not in p53-/- mice. CONCLUSIONS: Developmental RGC programmed cell death does not require p53. Selective overstimulation of the glutamate-dependent NMDA-receptor in adult mice activates a p53-dependent pathway of death in RGCs. The requirement for p53 is not absolute, however, because mice lacking this gene are able to execute an alternative pathway of cell death. Examination of the cleavage of PARP, which is a substrate for caspases, suggests that the p53-dependent pathway utilizes these proteases, but the p53-independent pathway does not.

Animals↗

PubMed1996

Globin gene switching. In vivo protein-DNA interactions of the human beta-globin locus in erythroid cells expressing the fetal or the adult globin gene program.

To characterize the protein-DNA interactions important for the developmental control of the human beta-globin locus, we analyzed by in vivo dimethyl sulfate footprinting erythroid cells expressing either the fetal or the adult globin developmental program. In the locus control region (LCR) of the beta-globin locus, in vivo footprints on NF-E2 (or AP-1) and GATA-1 motifs remained the same regardless of whether the fetal or the adult globin genes are expressed. In contrast, in vivo footprints on GT (CACCC) motifs differed between the cells expressing the fetal or the adult globin program. In promoter regions, the actively transcribed genes demonstrated extensive and consistent footprints over the canonical elements, such as CACCC and CCAAT motifs. The adult globin expressing cells displayed more extensive footprints than the fetal globin expressing cells in the 3' regulatory sequences of both the Agamma- and the beta-globin genes, suggesting a role of these 3' elements in beta-globin gene expression. Our results suggest that the bulk of protein-DNA interactions that underlies the developmental control of globin genes takes place in the gamma- and beta-globin gene promoters, and that GT motifs of the beta-globin locus LCR may play a role in the developmental regulation of human beta-globin gene expression, perhaps by increasing the probability of interaction of the LCR holocomplex with the fetal or the adult globin gene.

Adult↗

PubMed2000

Plant proteolytic enzymes: possible roles during programmed cell death.

Proteolytic enzymes are known to be associated with developmentally programmed cell death during organ senescence and tracheary element differentiation. Recent evidence also links proteinases with some types of pathogen- and stress-induced cell suicide. The precise roles of proteinases in these and other plant programmed cell death processes are not understood, however. To provide a framework for consideration of the importance of proteinases during plant cell suicide, characteristics of the best-known proteinases from plants including subtilisin-type and papain-type enzymes, phytepsins, metalloproteinases and the 26S proteasome are summarized. Examples of serine, cysteine, aspartic, metallo- and threonine proteinases linked to animal programmed cell death are cited and the potential for plant proteinases to act as mediators of signal transduction and as effectors of programmed cell death is discussed.

Apoptosis↗

PubMed1996

A relationship between apoptosis and flow during programmed capillary regression is revealed by vital analysis.

Previous analyses of developmentally programmed capillary regression suggested two distinct causes of vascular endothelial cell (VEC) death. The first appeared to be macrophage-dependent (Lang, R. A. and Bishop, M. J. (1993) Cell 74, 453-462) while the second was proposed to result from cessation of blood flow (Lang, R. A., Lustig, M., Francois, F., Sellinger, M. and Plesken, H. (1994). Development 120, 3395-3403). Combined, these analyses suggested a model in which initial, macrophage-mediated endothelial cell apoptosis blocked blood flow within a capillary segment and, as a consequence, caused apoptosis of all remaining cells in the affected segment. In the current study, we have tested this model using a new method that combines vital and histological analyses as a means of determining the fate of whole capillary segments and individual cells in vivo. This technique revealed that one of the first events in regression was the apoptosis of a single VEC in otherwise normal, flowing capillary segments (initiating apoptosis). These isolated, dying VECs projected into and restricted the capillary lumen, imposing either a temporary or permanent block to blood flow. Following cessation of flow, synchronous apoptosis of VECs occurred (secondary apoptosis). In addition, a quantitative analysis revealed a reciprocal relationship between plasma flow and VEC apoptosis. These observations are consistent with a model for capillary regression in which macrophages induce apoptosis in a limited number of VECs and, as a consequence of a block to blood flow, also cause apoptosis in those remaining.

Animals↗