Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “dimorphism”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 91 records · Page 5Linked to original sources

Sexual dimorphism in large-bodied primates: the case of the subfossil lemurs.

Large body size has evolved repeatedly in the order Primates, not merely among anthropoids but also among prosimians. Whereas high degrees of sexual size dimorphism characterize many of the large-bodied anthropoids, this is not the case for extinct large-bodied lemurs. This paper uses finite mixture analysis and other techniques to ascertain just how much skull length dimorphism might be embedded in the generally unimodal distributions of skull lengths of giant extinct lemurs from single localities, and then compares these results with known skull length dimorphisms in extant lemurs and large-bodied catarrhines. We show that low levels of skull length sexual dimorphism (or none at all) characterize subfossil lemurs, and we explore several possible explanations for this phenomenon. Traditional explanations of sexual size dimorphism generally focus on body size or mating systems. These are not sufficient to explain the variation in sexual dimorphism that can be observed in the order Primates.

Animals↗

Evidence for the existence of a sexually dimorphic nucleus in the preoptic area of the rat.

The volume of an intensely staining component of the preoptic area of the male rat is markedly larger than that of the female. Moreover, its volume in both sexes is altered by perinatal hormone exposure consistent with the view that this brain region undergoes hormone dependent sexual differentiation. The present study was carried out to determine if this sexually dimorphic area of the brain has a greater cell density than that of the surround, and if a unique population or distribution of cells, either within one sex or between males and females, characterized this region. A single coronal paraffin section (10 micrometer) through the approximate center of this sexually dimorphic area in four adult gonadectomized rats of each sex was evaluated systematically. Each cell was labelled as being inside or outside of the sexually dimorphic area. In addition to cell density per unit area the following parameters were evaluated through a closed-circuit video system: cell size, staining intensity, shape, and the presence of processes and of a nucleolus. The presence of a nucleolus was further used to identify neurons within the total population of almost 5000 cells that was evaluated. In both sexes, the sexually dimorphic area was characterized by a significantly increased cell density per unit area compared to that of the surround. On this basis, the term, the Sexually Dimorphic Nucleus of the Preoptic Area (SDN-POA) is proposed, for this region. Moreover, the SDN-POA of the male was characterized by increased neuronal density per unit area. The SDN-POA in the male was also found to contain larger cells and neurons, as determined by direct measurement of their greatest diameter, as well as a greater percentage of cells and neurons rated large on a three-point scale (small, medium, and large). No consistent differences in frequency distribution by stain intensity, shape, or the presence of cell processes were found to characterize the SDN-POA or contribute to the sexual dimorphism. It is concluded that the marked sex difference in the volume of the SDN-POA is due principally to an increase in the male of the total area of higher cell and neuronal density. However, the present results do not eliminate the possibility that more subtle differences in neuronal characteristics may exist in the SDN-POA.

Animals↗

Source of sexually dimorphic galanin-like immunoreactive projections in the teleost fish Poecilia latipinna.

A galanin-like peptide has a sexually dimorphic distribution in the teleost fish, the sailfin molly. An extensive system of galanin-like immunoreactive (GAL-LI) fibers has been described in the brainstem and spinal cord of the male molly, which is absent in the female (Cornbrooks and Parsons, companion paper). As GAL-LI in the mammalian spinal cord has been localized to neurons of origin in the dorsal root ganglia and dorsal and ventral horns, the present study was undertaken to determine whether the sexually dimorphic GAL-LI in the male molly may originate in part from corresponding sources in this species. Colchicine treatments of the spinal cord and dorsal root ganglia did not result in GAL-LI staining in neuronal somata in these regions. Following complete transection of the spinal cord and at any level of the spinal cord, there was a complete absence of GAL-LI caudal to the lesion site. In fish that received unilateral spinal transection, there was a loss of GAL-LI ipsilateral and caudal to the lesion. Finally, in fish that received lesions in the rostral hypothalamus, there was a complete loss of GAL-LI in the sexually dimorphic fiber system in the brainstem and spinal cord, but not in non-dimorphic GAL-LI regions of the brainstem. Thus the sexually dimorphic fiber system in the male molly may originate in neurons of the preoptic nucleus that are sexually dimorphic for a GAL-LI peptide. This preoptico-spinal pathway may mediate sex-specific behaviors in this species.

Animals↗

Dimorphic Alu element located between the TFIIH and CDSN genes within the major histocompatibility complex.

Most Alu members of the large SINE family are fixed within the human genome but some younger mobile members are dimorphic, that is, they are either present or absent in the genome. Four different dimorphic Alu insertions have been identified and characterized previously within the class I region of the major histocompatibility complex (MHC). Here we report on (i) the identification and characterization of a new dimorphic Alu insertion, AluyTF, located between the transcription factor II H (TFIIH) and corneodesmosin (CDSN) genes within a region of the MHC that is telomeric of the human leukocyte antigen type B (HLA-B) locus and centromeric of the HLA-A locus, (ii) the haplotypic relationships between the AluyTF dimorphism and the HLA-A and -B loci within a panel of 48 IHW cell-lines representing at least 36 different HLA class I haplotypes, (iii) the AluyTF genotype, allele and haplotype frequencies present in the Australian caucasian and Japanese populations, and (iv) the frequency of association between the AluTF dimorphisms and HLA-A and -B alleles in 108 Australian caucasians and 99 Japanese. The AluyTF insertion was present at 27% in the IHW cell lines, and the gene frequency was 0.107 and 0.083 in the Australian caucasian and Japanese population, respectively. The Alu haplotype frequencies constructed from four different dimorphic Alu loci including AluyTF within the MHC were not significantly different (p > 0.05) between the two populations. There were no significant associations between the Alu insertion and either the HLA-A or -B alleles except for a moderately strong association with HLA-A29 in the Australians (71.7%). This polymorphic AluyTF element, along with the four other previously described polymorphic Alu elements within the class I region of the MHC, will be useful lineage and linkage markers in human population studies and for elucidating the evolution of HLA class I haplotypes.

Alu Elements↗

Pelvic growth: ontogeny of size and shape sexual dimorphism in rat pelves.

The mammalian pelvis is sexually dimorphic with respect to both size and shape. Yet little is known about the differences in postnatal growth and bone remodeling that generate adult sexual dimorphism in pelvic bones. We used Sprague-Dawley laboratory rats (Rattus norvegicus), a species that exhibits gross pelvic size and shape dimorphism, as a model to quantify pelvic morphology throughout ontogeny. We employed landmark-based geometric morphometrics methodology on digitized landmarks from radiographs to test for sexual dimorphism in size and shape, and to examine differences in the rates, magnitudes, and directional patterns of shape change during growth. On the basis of statistical significance testing, the sexes became different with respect to pelvic shape by 36 days of age, earlier than the onset of size dimorphism (45 days), although visible shape differences were observed as early as at 22 days. Males achieved larger pelvic sizes by growing faster throughout ontogeny. However, the rates of shape change in the pelvis were greater in females for nearly all time intervals scrutinized. We found that trajectories of shape change were parallel in the two sexes until age of 45 days, suggesting that both sexes underwent similar bone remodeling until puberty. After 45 days, but before reproductive maturity, shape change trajectories diverged because of specific changes in the female pelvic shape, possibly due to the influence of estrogens. Pattern of male pelvic bone remodeling remained the same throughout ontogeny, suggesting that androgen effects on male pelvic morphology were constant and did not contribute to specific shape changes at puberty. These results could be used to direct additional research on the mechanisms that generate skeletal dimorphisms at different levels of biological organization.

Aging↗

Sexual dimorphism in the hypothalamo-pituitary-adrenal (HPA) axis and TNFalpha responses to phospholipase A2-related neurotoxin (from crotalus durissus terrifcus) challenge.

Neuroendocrine-immune interactions are vital for the individual's survival in certain physiopathological conditions such as sepsis and tissular injury. It is known that several snake venoms (SV) are potent neurotoxic compounds and that their main component is a specific phospholipase type 2 (PLA2). It has been recently described that the venom from crotalus durissus terrificus (SV) possesses a cytotoxic effect in different in vitro and in vivo animal models. In the present study we investigated whether SV is able to stimulate both TNFalpha and neuroendocrine functions in a sexual dimorphic fashion. For this purpose the modulatory role of endogenous sex steroids during neurotoxemia was evaluated. Our results indicate that SV (25 microg/animal) stimulates the hypothalamo-pituitary-adrenal axis and TNFalpha secretion when administered (ip) to adult male mice, such responses were characterized by a time-related enhance in plasma glucose, ACTH, corticosterone and TNFalpha levels. SV-stimulated glycemia, corticosteronemia and adrenal glucocorticoid were sexually dimorphic. Twenty-day gonadectomized mice showed a similar sexual dimorphism to that found in intact animals, however, they additionally showed a sexual dimorphic pattern in cytokine release in plasma 30 min post-SV. Estradiol (E2) treatment, in gonadectomized mice, abolished some characteristics of the sexual dimorphism, such as hyperglycemia, hypercorticosteronemia and hypercytokinemia. Finally, in vitro experiments indicate that: a) gonadectomy increased spontaneous and SV-stimulated cytokine output by incubated peripheral mononuclear cells (PMNC), regardless of the sex; and b) despite E2 treatment, in gonadectomized, did not modify the pattern of basal and SV-elicited TNFalpha secretion induced by orchidectomy, fully reversed the enhance in basal and SV-stimulated cytokine release found after ovariectomy alone. Our results further indicate that neurotoxemia, due to SV challenge, induces several symptoms common to those of inflammatory stress; they also strongly support that both gender and endogenous sex steroids are responsible for neuroendocrine-immunological sexual dimorphism.

Adrenal Glands↗

Sexual dimorphism and species differences in the neurophysiology and morphology of the acoustic communication system of two neotropical hylids.

We examined auditory tuning and the morphology of the anatomical structures underlying acoustic communication in female Hyla microcephala and H. ebraccata and compared our findings to data from a previous study (Wilczynski et al. 1993) in which we showed species differences in the traits that in males relate to differences in the species-typical calls. Female species differences in the best excitatory frequency (BEF) of the basilar papilla (BP) were similar to the differences seen in males, and females had a significantly lower BEF in H. ebraccata, but not H. microcephala. In both species, females had lower BP thresholds. Snout-vent length, head width, and tympanic membrane diameters were sexually dimorphic in both species and larger in females, whereas laryngeal components were sexually dimorphic and larger in males. Middle and inner ear volumes were not sexually dimorphic. Despite the significant species differences in laryngeal morphology seen in males, female larynges are not significantly different. Furthermore, the interaction of species and sex differences resulted in significantly different degrees of sex dimorphism in the species, particularly for the larynx, which is more sexually dimorphic in H. microcephala, and measures of body size, which are more dimorphic in H. ebraccata.

Amphibians↗

Distribution of alpha 2-adrenergic receptors in the brain of the Japanese quail as determined by quantitative autoradiography: implications for the control of sexually dimorphic reproductive processes.

With the use of [3H]p-aminoclonidine (PAC), alpha 2-adrenergic binding sites were mapped in the brain of the Japanese quail (Coturnix coturnix japonica). The sites were labeled with the use of in vitro quantitative autoradiography. Special attention was given to areas implicated in the control of sexually dimorphic reproductive processes including sexual behavior. Preliminary competition experiments found that [3H]PAC binding on tissue sections exhibited a pharmacology appropriate to the alpha 2 receptor. Binding sites were found to be heterogeneously distributed throughout the brain. Some of the highest levels of specific binding were found in several areas regulating reproductive function such as the preoptic area, the supraoptic nucleus, the infundibulum, and the medial mammillary nucleus of the infundibulum. [3H]PAC labeled precisely the morphologically dimorphic preoptic medial nucleus but no sexual dimorphism in density of receptor binding was identified. However, dimorphism in density of receptor binding was identified in two areas: the medial mammillary nucleus and the mesencephalic intercollicular nucleus. The former area appears to be involved in the regulation of gonadotrophin secretion and the latter area has been implicated in the control of vocal behavior. These neurochemical dimorphisms may contribute to the regulation of two sexually dimorphic reproductive processes, gonadotropin secretion and courtship vocalizations.

Adrenergic alpha-Agonists↗

Dimorphic sequences of rap-1 genes encode B and CD4+ T helper lymphocyte epitopes in the Babesia bigemina rhoptry associated protein-1.

The rhoptry-associated protein-1 (RAP-1) of Babesia bigemina induces protective immune responses in cattle and contains neutralization-sensitive B cell epitopes. RAP-1 variants containing blocks of sequence dimorphism in the amino and carboxy terminal ends are encoded by four nonallelic genes in B. bigemina. Epitopes recognized by RAP-1 specific monoclonal antibodies (MAbs) and bovine CD4+ T cell clones were mapped to determine whether these epitopes are localized in the amino and carboxy terminal dimorphic regions. Four B cell epitopes, including a neutralization-sensitive epitope, required both the amino terminal variant type 1 (NT-1) and non-dimorphic sequences for conformation. Intrachain disulfide bonds were required for at least one of these epitopes, since reduction and alkylation of cysteine residues abolished MAb binding. A fifth B cell epitope was mapped to the carboxy terminal variant type 1 (CT-1). As expected, the neutralizing MAb and two other MAbs requiring NT-1 for epitope binding recognized only the two RAP-1 variants with the NT-1 sequence, while the MAb binding an epitope in CT-1 did not bind RAP-1 variants with CT-2. In contrast, the fourth MAb requiring NT-1 for binding recognized all rap-1 gene products, indicating that dimorphic residues are not part of the epitope recognized by this MAb. Bovine CD4+ T cell clones characterized previously as responding in a strain dependent fashion recognized at least one epitope in CT-1, and did not cross-react with CT-2. A second group of bovine CD4+ T cell clones that responded to multiple parasite strains recognized an epitope in a non-dimorphic region of RAP-1. These data indicate that dimorphic regions of RAP-1 encode unique B and T helper lymphocyte epitopes and may be required for enhanced protective immune responses in cattle.

Animals↗

Ontogeny, sex dimorphism, and neonatal sex hormone determination of synapse-associated messenger RNAs in rat brain.

Sex hormones influence neurite outgrowth and synaptogenesis in certain hormone-dependent areas of the rat brain during neonatal development. These alterations are thought to mediate changes in brain structure and function between the sexes. Growth-associated protein 43 kDa (GAP-43) gene expression is estrogen-regulated in the adult ventromedial hypothalamus (VMH) and sexually dimorphic (M:F = 1.8:1) in adult cortex (CTX). Such effects intimate hormonal regulation of synaptic plasticity. To investigate the nature of these dimorphisms, the present study examined the ontogeny of expression of mRNAs encoding 3 neural-specific proteins: GAP-43, SCG10, and synaptosomal-associated protein 25 kDa (SNAP-25); and glyceraldehyde-3-phosphate dehydrogenase (GAPDH), in the VMH and CTX; and also the effects of altering the neonatal sex hormonal milieu on the development of these adult dimorphisms. Levels of specific mRNAs in VMH and CTX were quantitated by slot-blot hybridization in rats of both sexes at different postnatal ages. To determine the involvement of neonatal sex hormones on the levels of these mRNAs, male neonatal rat pups were treated with an estrogen receptor antagonist or an aromatase inhibitor, and neonatal female pups were treated with testosterone or estrogen prior to slot-blot evaluations in adulthood. In VMH, GAP-43 mRNA levels were high on days P1 and P4 with a 3-fold decrease by day P23; in CTX, GAP-43 mRNA first increased by day P11, then fell to baseline by day P23. In VMH, SCG10 mRNA showed only small increases with time; but in CTX, there was a 5-fold drop from days P4 to P23. In VMH, SNAP-25 mRNA was low and changed only slightly; but in CTX there was a 5-fold increase between days P4 and P60. At birth, there was no sex dimorphism in either VMH or CTX, but the levels of all 3 neural-specific mRNAs were sexually dimorphic in adult CTX (M:F = 1.76 for GAP-43, 1.46 for SCG10, 1.44 for SNAP-25). GAPDH mRNA levels were regulated developmentally in VMH and CTX, but there was no sex dimorphism in either area. In male rats who received either an estrogen antagonist or aromatase inhibitor at birth, the CTX GAP-43 and SNAP-25 mRNA levels fell by 30%, to levels similar to untreated females. Conversely, in female rats, neonatal treatment with either testosterone or estrogen increased GAP-43 and SNAP-25 mRNA levels by about 30%, to levels similar to the untreated adult male. SCG10 levels did not demonstrate neonatal hormonal dependence.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

Bootstrap tests of significance and the case for humanlike skeletal-size dimorphism in Australopithecus afarensis.

Most estimates of sexual size dimorphism in Australopithecus afarensis indicate that this early hominin was more dimorphic than modern humans. In contrast, a recent study reported that size variation in A. afarensis, as represented by postcranial remains from Hadar and Maka, Ethiopia, is statistically most similar to that of modern humans, indicating a humanlike level of sexual dimorphism. Here, we evaluate the evidence for humanlike dimorphism in A. afarensis. We argue that statistical support for this claim is not as robust as has been asserted for the following reasons: (1) the analysis from which the claim was derived does not distinguish the A. afarensis sample from either the human or chimpanzee samples; (2) for some of the comparisons made, the A. afarensis sample cannot be distinguished from the Gorilla sample using two-tailed tests; and (3) the A. afarensis postcranial sample used in the analysis may contain more male than female specimens, which precludes a straightforward interpretation of the statistical results. Thus, support for humanlike dimorphism is equivocal, and a greater level of dimorphism cannot be ruled out.

Animals↗

Visualizing sexual dimorphism in the brain.

Sexually dimorphic behaviors are likely to involve neural pathways that express the androgen receptor (AR). We have genetically modified the AR locus to visualize dimorphisms in neuronal populations that express AR. Analysis of AR-positive neurons reveals both known dimorphisms in the preoptic area of the hypothalamus and the bed nucleus of the stria terminalis as well as novel dimorphic islands in the basal forebrain with a clarity unencumbered by the vast population of AR-negative neurons. This genetic approach allows the visualization of dimorphic subpopulations of AR-positive neurons along with their projections and may ultimately permit an association between neural circuits and specific dimorphic behaviors.

Animals↗

Adult gonadal hormones selectively regulate sexually dimorphic quantitative traits observed in experimental allergic encephalomyelitis.

Experimental allergic encephalomyelitis (EAE) and multiple sclerosis (MS) are characterized by strong sexual dimorphisms, many of which may be due to genetically controlled sex hormone effects on the immune system, the central nervous system (CNS), or both. In the present study we used 487 gonadectomized and 376 intact age-matched F(2) mice generated through crosses of B10.S/SgMcdJ and SJL/J mice to assess the role of adult gonadal hormones in regulating clinical and histopathological quantitative traits (QT) associated with EAE in the context of genetic heterogeneity. We found that gonadectomy resulted in different effects, depending on the QT and the sex of the mouse. Ovariectomized mice on average had lower cumulative clinical disease scores, shorter duration of clinical signs, and increased peak disease scores. This trend was accompanied by a significant increase in the incidence of acute, progressive EAE which is more frequently seen in intact and orchiectomized males. Although spinal cord (SC) inflammation was the better predictor of clinical signs of EAE in both sexes, ovariectomized females had considerable reductions in nearly all histopathological QT in both the brain and SC. Orchiectomy resulted in modestly significant increases in disease severity and peak score and earlier onset of clinical signs. With the exception of SC demyelination and lesion scores, orchiectomy had no effect on histopathological QT. Importantly, gonadectomy reduced but did not completely abolish any of the sexually dimorphic clinical QT seen in intact mice. It did however, lead to a significant sexual dimorphism in incidence and severity not seen in intact mice. For histopathological QT, no sexual dimorphism was detected for brain lesions in either intact or gonadectomized mice. In contrast, SC histopathological QT exhibited significant sexual dimorphisms, which were impacted by gonadectomy. The results from this study indicate that within the context of genetic heterogeneity, circulating gonadal hormones influence both clinical and histopathological QT in this model of MS, but they do not solely account for the sexual dimorphisms seen in these traits. Thus, additional mechanisms must play a role in regulating gender differences in autoimmune disease of the CNS.

Animals↗

Leptin's sexual dimorphism results from genotype by sex interactions mediated by testosterone.

OBJECTIVE: Recent studies have reported the existence of marked sexual dimorphism in serum leptin levels in humans, with women having approximately three times the levels of men. As we have shown for other measures of adiposity, such sexual dimorphism can arise from a special case of genotype by environment interaction, that of genotype by sex interaction. RESEARCH METHODS AND PROCEDURES: Using maximum likelihood-based variance decomposition techniques, we examined the genetic and environmental architecture of sexual dimorphism in serum leptin levels in 1147 Mexican Americans from the San Antonio Family Heart Study. RESULTS: Both the genetic and environmental variances for this trait differed significantly between the sexes (p < 0.001 and p < 0.01, respectively), with women displaying larger values for both components. We found significant evidence that different genes influence variation in serum leptin levels between the two sexes (p = 0.05). Furthermore, this pattern of sexual dimorphism in serum leptin levels persisted even after accounting for the effects of either the percentage of body fat or total body fat. However, this pattern of sexual dimorphism was eliminated after accounting for the effects of testosterone. DISCUSSION: These findings suggest that the sexual dimorphism seen in leptin levels is not simply explained as differences in total adiposity between the sexes. We conclude that the genes, which influence variation in serum leptin levels, are differentially expressed depending on sex, and that the sexes also show differences in response of the expression of this obesity-related trait to unmeasured residual effects.

Adipose Tissue↗

Beta 2-adrenergic receptor regulation of human neutrophil function is sexually dimorphic.

While the mechanisms underlying the marked sexual dimorphism in inflammatory diseases are not well understood, the sexually dimorphic sympathoadrenal axis profoundly affects the inflammatory response. We tested whether adrenergic receptor-mediated activation of human neutrophil function is sexually dimorphic, since neutrophils provide the first line of defense in the inflammatory response. There was a marked sexual dimorphism in beta(2)-adrenergic receptor binding, using the specific beta(2)-adrenergic receptor ligand, [(3)H]-dihydroalprenolol, with almost three times more binding sites on neutrophils from females (20,878 +/- 2470) compared to males (7331 +/- 3179). There was also a marked sexual dimorphism in the effects of isoprenaline, a beta-adrenergic receptor agonist, which increased nondirected locomotion (chemokinesis) in neutrophils obtained from females, while having no effect on neutrophils from males. Isoprenaline stimulated the release of a chemotactic factor from neutrophils obtained from females, but not from males. This chemotactic factor acts on the G protein-coupled CXC chemokine receptor 2 (CXCR2) chemokine receptor, since an anti-CXCR2 antibody and the selective nonpeptide CXCR2 antagonist SB225002, inhibited chemotaxis produced by this factor. While interleukin- (IL-) 8 is a principal CXCR2 ligand, isoprenaline did not produce an increase in IL-8 release from neutrophils. IL-8-induced chemotaxis was inhibited in a sexually dimorphic manner by isoprenaline, which also stimulated release of a mediator from neutrophils that induced chemotaxis, that was inhibited by anti-CXCR2 antibodies. These findings indicate an important role for adrenergic receptors in the modulation of neutrophil trafficking, which could contribute to sex-differences in the inflammatory response.

Adrenergic beta-2 Receptor Agonists↗

Association of the angiotensin-converting enzyme (ACE) gene G2350A dimorphism with essential hypertension.

Although the angiotensin converting enzyme (ACE) is a strong candidate gene for hypertension, the extensively studied insertion-deletion dimorphism in intron 16 was not found to be associated with it. Several new polymorphisms in the ACE gene were identified, among which a dimorphism in exon 17, ACE G2350A, has a significant effect on plasma ACE concentrations. To assess the value of genotyping the ACE G2350A dimorphism in a genetically homogeneous population, we carried out a retrospective, case-control study of dimorphism G2350A for a putative association with essential hypertension (EH) in a Gulf population (Emirati)--an ethnic group characterized by no alcohol intake and no cigarette smoking. We investigated a sample population of 254 Emirati, comprising 136 normotensive controls, and 118 patients with clinical diagnoses of EH. ACE G2350A alleles were visualized by assays based on polymerase chain reaction and restriction endonuclease analysis. The ACE G2350A dimorphism showed an association with EH (chi2=6.71, 2 df, P=0.05). Further analysis revealed that the ACE G/G 2350 genotype was positively associated (OR=1.06-3.07, P=0.02) with EH. This is the first association study of the ACE G2350A dimorphism with EH, and the positive result might indicate that ACE could be a QTL for EH as originally thought.

Adult↗

The phylogenetic basis of sexual size dimorphism in orb-weaving spiders (Araneae, Orbiculariae).

Extreme sexual body size dimorphism (SSD), in which males are only a small fraction of the size of the females, occurs only in a few, mostly marine, taxonomic groups. Spiders are the only terrestrial group in which small males are relatively common, particularly among orb-weavers (especially in the families Tetragnathidae and Araneidae) and crab spiders (Thomisidae). We used a taxonomic sample of 80 genera to study the phylogenetic patterns (origins and reversals) of SSD in orb-weaving spiders (Orbiculariae). We collected and compiled male and female size data (adult body length) for 536 species. Size data were treated as a continuous character, and ancestral sizes, for males and females separately, were reconstructed by using Wagner parsimony on a cladogram for the 80 genera used in this study. Of these 80 genera, 24 were female-biased dimorphic (twice or more the body length of the male); the remaining 56 genera were monomorphic. Under parsimony only four independent origins of dimorphism are required: in the theridiid genus Tidarren, in the distal nephilines, in the "argiopoid clade," and in the araneid genus Kaira. Dimorphism has reversed to monomorphism at least seven times, all of them within the large "argiopoid clade." The four independent origins of dimorphism represent two separate instances of an increase in female size coupled with a decrease of male size (involving only two genera), and two separate instances of an increase in female size with male size either remaining the same or increasing, but not as much as females (involving 30 genera). In orb-weaving spiders, far more taxa are sexually dimorphic as a result of female size increase (22 genera) than as a result of male size decrease (two genera). SSD in orb-weaving spiders encompasses several independent evolutionary histories that together suggest a variety of evolutionary pathways. This multiplicity strongly refutes all efforts thus far to find a general explanation for either the origin or maintenance (or both) of SSD, because the different pathways very likely will require distinctly different, possibly unique, explanations. Each pattern must be understood historically before its origin and maintenance can be explained in ecological and evolutionary terms. The most frequently cited example of male dwarfism in spiders, the golden orb-weaving spider genus Nephila (Tetragnathidae), is in fact a case of female giantism, not male dwarfism.

Animals↗

Pupal remodeling and the development and evolution of sexual dimorphism in horned beetles.

Horns or hornlike structures in beetles have become an increasingly popular study system for exploring the evolution and development of secondary sexual trait diversity and sexual dimorphisms. The horns of adult beetles originate during a rapid growth phase during the prepupal stage of larval development, and differential activation of growth during this time is either implicitly or explicitly assumed to be the sole mechanism underlying intra- and interspecific differences in adult horn expression. Here I show that this assumption is not based on developmental reality. Instead, after their initial prepupal growth phase, beetle horns are extensively remodeled during the subsequent pupal stage via sex- and size-dependent resorption of horn tissue. I show that adult sexual dimorphism in four Onthophagus species is shaped partly or entirely by such pupal remodeling rather than by differential growth. Specifically, I show that after a sexually monomorphic growth phase, differential pupal horn resorption can generate both regular and reversed sexual dimorphism. Furthermore, I show that in cases in which initial growth is already dimorphic, pupal horn resorption can both magnify and reverse initial dimorphism resulting from differential growth. Finally, I show that complete resorption of pupal horns in both sexes can remove any trace of horn expression from all resulting adults. In such species, examination of adults only would result in the false conclusion that this species lacks the ability to develop a horn. Instead, such species appear to differ from those with sexually dimorphic adults merely in that they activate pupal horn resorption in both sexes rather than in just one. Combined, these results suggest that pupal remodeling of secondary trait expression is taxonomically widespread, at least among Onthophagus species, and is developmentally extensive and remarkably evolutionarily labile. These results have immediate implications for reconstructing the evolutionary history of horned beetles and the role of developmental processes in guiding evolutionary trajectories. I use these results to revise current understanding of the evolutionary developmental biology of secondary sexual traits in horned beetles in particular and holometabolous insects in general. The results presented here seriously call into question whether descriptions of adult diversity patterns alone suffice for meaningful inferences toward understanding the developmental and evolutionary origin of these patterns. These results illustrate that a lasting integration of development into an evolutionary framework must integrate development as a process rather than define it solely by some of its products.

Animal Structures↗