Do Kin Selection and Intra-Sexual Selection Operate in Spider Mites?

Between the two subsocial spider mites, Schizotetranychus longus Saito and S. miscanthi Saito, a big difference exists in male reproductive behavior. The males of the former species have an extraordinarily mild relationship with conspecific males, whereas those of the latter species show mortal aggression against conspecific males. Field and experimental observations on the structure of mating populations showed that S. longus is under inbreeding conditions because of a lack of males in early spring, whereas S. miscanthi is under outbreeding conditions. Therefore, I hypothesized that the difference in male antagonism between the two species may reflect the difference in relatedness of males, that is, it has evolved by kin selection. The recent discovery of two clinal trends in male–male aggression in S. miscanthi provided evidence in favour of this hypothesis. Furthermore, a correlation analyses between experimentally evaluated male aggression and distribution patterns of males in the field indicated that the variation in male antagonism is actually reflected in field populations. Based on these studies, I discuss the solidity of the kin-selection hypothesis. Lastly I address how spider mites are fruitful model animals for conducting behavioral, ecological and genetic studies to understand the evolution of haplo-diploidy.     

Insect Choice and Floral Size Dimorphism: Sexual Selection or Natural Selection?

In considerations of sexual floral size dimorphism, there is a conflict between sexual selection theory, which predicts that larger floral displays attract more pollinators, and optimality theory—particularly the ideal free distribution—which predict that pollinators' visits should match nutritional rewards. As an alternate explanation of this dimorphism, Müller reported that pollinators tend to visit larger male flowers before visiting smaller female flowers, thereby promoting effective pollination. To investigate optimality predictions, I offered pollinators a choice between smaller, less numerous, but more rewarding flowers; and larger, more numerous, but less rewarding flowers. Foragers initially favored the larger and more numerous flowers, but rapidly shifted preferences to conform with the predictions of the ideal free distribution. To test Müller's hypothesis, I offered pollinators choices between larger and smaller corollas of equal caloric reward. Results showed that although pollinators tended to visit larger corollas first, they did not visit them more often. These experiments highlight the need for further investigation into the tradeoff between natural and sexual selection, and their respective influences in pollination ecology.     

How Do Astrocytes Participate in Neural Plasticity?

Work over the past 20 years has implicated electrically nonexcitable astrocytes in complex neural functions. Despite controversies, it is increasingly clear that many, if not all, neural processes involve astrocytes. This review critically examines past work to identify the commonalities among the many published studies of neuroglia signaling. Although several studies have shown that astrocytes can impact short-term and long-term synaptic plasticity, further work is required to determine the requirement for astrocytic Ca²⁺ and other second messengers in these processes. One of the roadblocks to the field advancing at a rapid pace has been technical. We predict that the novel experimental tools that have emerged in recent years will accelerate the field and likely disclose an entirely novel path of neuroglia signaling within the near future.The year 2014 represents the 20th anniversary of a pair of papers published by the writers that provided the first indication that astrocytes actively signal to neurons, and that these glial cells have the potential to be participants in the control of neural circuit function and behavior (Nedergaard 1994; Parpura et al. 1994). Although we have taken independent paths, we come together on this anniversary to discuss what we have learned since 1994, where we see the field progressing, and, finally, to discuss some key steps that we believe should be taken in the next decade to begin to further clarify the diverse roles that astrocytes play in brain function in health and disease.Without knowledge of one another’s work, we published a pair of papers that provided the first demonstration that physiological changes in astrocytes influence neurons: stimulated Ca²⁺ changes in astrocytes led to delayed Ca²⁺ responses in neurons (Nedergaard 1994; Parpura et al. 1994). To set the backdrop to these studies, this was a period of explosive growth in Ca²⁺ imaging that resulted from the availability of fluorescent Ca²⁺ indicators and sensitive cameras to permit low-light-level imaging of intracellular biochemistry. As a consequence, there had been several recently published studies revealing that astrocytes show Ca²⁺ elevations in response to mechanical contact or even to the addition of neurotransmitters, such as glutamate (Cornell-Bell et al. 1990). However, the functional downstream consequences were unknown. In our studies, which used a combination of different stimuli—mechanical, optical, as well as a chemical transmitter bradykinin—we were able to show a robust impact of the astrocytic Ca²⁺ signal on the adjacent neurons (Nedergaard 1994; Parpura et al. 1994). Despite differences in mechanistic conclusions, these papers stimulated revised thinking about roles of astrocytes in the brain—perhaps these glial cells were actively signaling, albeit on a slower time scale, to modulate neurons, circuits, and, ultimately, behavior.The subsequent two decades have been spent examining the signaling of astrocytes to neurons in more intact systems. As a consequence of this work, it is clear that astrocytes play critical roles in actively modulating brain function, although we are still putting the pieces of the puzzle in place to understand where, when, and how this process occurs naturally in vivo and when dysfunction can lead to disorders of the brain.The field has gone through an explosive growth that has consisted of several phases. Initially, there was the dish phase in which the potential of the astrocyte was revealed in cell culture. These studies were essential as they captured our imagination and stimulated new thinking; however, they were limited by the fact that the properties of astrocytes can be different in vitro and in vivo. Next, we had the in situ phase, in which we asked whether similar processes could be detected in situ in acutely isolated brain slices. Then we began asking about roles in vivo through Ca²⁺ imaging together with two-photon microscopy as well as with molecular genetic alterations to permit the inhibition and stimulation of astrocytes. Each of these phases has offered unique insights, challenges, and opportunities for the field.Through all of these phases, an emergent picture is developing in which it is without doubt that astrocytes play important roles in vivo but that the mechanisms are so diverse and complex that an understanding is still to emerge.Some of the major challenges that we have faced and continue to face include: What are the endogenous signals of these glial cells? How can we stimulate astrocytes in a physiologically relevant manner? How can we inhibit astrocytes to determine when they are needed for brain function? And last, but by no means least, how diverse are astrocytes?We are still at the early days of understanding astrocytes, and patience regarding functional interpretation is required. We make this statement because there have been apparently contradictory conclusions drawn from different studies. The individual observations are important as they help provide a fuller picture of the biology of these complex cells. However, the jury still needs further evidence before definitive conclusions can be drawn. For example, a plethora of studies have shown that Ca²⁺ signals stimulate gliotransmission and the consequent modulation of neurons and synapses (see Agulhon et al. 2010), the field was rocked. We do not question the data of the study; instead, we believe this is an important piece of information that ultimately needs to be put in context. In contrast, additional studies have shown that IP₃ receptors are important for other aspects of astrocyte-induced synaptic modulation. A more recent study has shown that, in addition to Ca²⁺ release from internal stores, the influx of Ca²⁺ through transient receptor potential (TRP) channels is important for gliotransmission (Shigetomi et al. 2013). Clearly, such influx sites were unlikely to have been affected by the IP₃R₂ knockout and were shown to regulate d-serine release from the astrocyte. Another piece of the puzzle is added. Undoubtedly, there will be further twists and turns, but that is the joy of discovery, and it should be embraced.

Table 1.

Effect of Ca²⁺ signaling on excitatory or inhibitory potentials, slow inward current, synaptic failure, or neural bistability

Structural Plasticity in Human Heterochromatin Protein 1β

As essential components of the molecular machine assembling heterochromatin in eukaryotes, HP1 (Heterochromatin Protein 1) proteins are key regulators of genome function. While several high-resolution structures of the two globular regions of HP1, chromo and chromoshadow domains, in their free form or in complex with recognition-motif peptides are available, less is known about the conformational behavior of the full-length protein. Here, we used NMR spectroscopy in combination with small angle X-ray scattering and dynamic light scattering to characterize the dynamic and structural properties of full-length human HP1β (hHP1β) in solution. We show that the hinge region is highly flexible and enables a largely unrestricted spatial search by the two globular domains for their binding partners. In addition, the binding pockets within the chromo and chromoshadow domains experience internal dynamics that can be useful for the versatile recognition of different binding partners. In particular, we provide evidence for the presence of a distinct structural propensity in free hHP1β that prepares a binding-competent interface for the formation of the intermolecular β-sheet with methylated histone H3. The structural plasticity of hHP1β supports its ability to bind and connect a wide variety of binding partners in epigenetic processes.     

Selection for the α-Thalassemia Genes

Extremely high incidences of single and double deletions of α-globin genes are known among Asian populations. To study possible mechanisms for the maintenance of such deletions, mathematical analyses have been conducted. It has been shown that a stable polymorphism can be achieved easily through heterozygote advantage using deterministic models. The results strongly suggest that high incidences of single and double deletion of α-globin genes among Asian populations are maintained by some type of heterozygote advantage.     

Plasticity of the Electrical Connectome of C. elegans

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Promotion of Neuronal Plasticity by (−)-Epigallocatechin-3-Gallate

The consumption of (−)-epigallocatechin-3-gallate (EGCG), the major polyphenolic compound found in green tea, has been associated with various neurological benefits including cognitive improvement. The physiological basis for this effect is unknown. In this study, we used synaptic transmission between the CA3 and CA1 regions (Schaffer collateral) of the mouse hippocampus to examine the effects of EGCG on neuronal plasticity. We found that the level of high frequency stimulation-evoked long-term potentiation (LTP) was significantly enhanced when hippocampal slices were pre-incubated with 10 μM EGCG for 1 h prior to the experiment. EGCG incubation also enabled hippocampal slices prepared from Ts65Dn mice, a Down syndrome mouse model deficient in LTP, to express LTP to a level comparable to the normal controls. EGCG treatment did not alter the degree of pair-pulse inhibition; therefore, the enhancement effect of EGCG is unlikely to involve the attenuation of this inhibitory mechanism.     

Examination “Selection Pressures” in Biology

Class Work with Fungi. H. A. DADE and JEAN GUNNELL. Pp. 64. London: Commonwealth Mycological Institute, Kew. 1969. 10s. Review by B. M. Jones

The Insects: Structure and Function. R. F. CHAPMAN. Pp. xiii + 819 + 509 figs. London: The English Universities Press Ltd., 1969. £4.25. Review by T. G. Onions

An Introduction to the Principles of Plant Physiology. WALTER STILES and E. C. COCKING. Pp. 633. London: Methuen &; Co., Ltd. Third edition, 1969. 168s. Review by B. M. Jones

Background Notes to the Study of Human Biology for Nurses. T. ROBERTS. Pp. 80. London: Edward Arnold. Semistiff Back, 10s. (50p.). Review by J. H. Elliott     

Autophagy and Self-Preservation: A Step Ahead from Cell Plasticity?

Silencing the SPINK-related gene Kazal1 in hydra gland cells induces an excessive autophagy of both gland and digestive cells, leading to animal death. Moreover, during regeneration, autophagosomes are immediately detected in regenerating tips, where Kazal1 expression is lowered. When Kazal1 is completely silenced, hydra no longer survive the amputation stress (Chera S, de Rosa R, Miljkovic-Licina M, Dobretz K, Ghila L, Kaloulis K, and Galliot B. Silencing of the hydra serine protease inhibitor Kazal1 gene mimics the human Spink1 pancreatic phenotype. J Cell Sci 2006; 119:846-57). These results highlight the essential digestive and cytoprotective functions played by Kazal1 in hydra. In mammals, autophagy of exocrine pancreatic cells is also induced upon SPINK1/Spink3 inactivation, whereas SPINK3 is activated in injured pancreatic cells. Hence SPINKs, by preventing an excessive autophagy, appear to act as key players of the stress-induced self-preservation program. In hydra, this program is a prerequisite to the early cellular transition, whereby digestive cells of the regenerating tips transform into a head-organizer center. Enhancing the self-preservation program in injured tissues might therefore be the condition for unmasking their potential cell and/or developmental plasticity.

Addendum to:

Silencing of the Hydra Serine Protease Inhibitor Kazal1 Gene Mimics the HumanSpink1 Pancreatic Phenotype

S. Chera, R. de Rosa, M. Miljkovic-Licina, K. Dobretz, L. Ghila, K. Kaloulis and B. Galliot

J Cell Sci 2006; 119:846-57     

Cerebellar Motor Learning: When Is Cortical Plasticity Not Enough?

Classical Marr-Albus theories of cerebellar learning employ only cortical sites of plasticity. However, tests of these theories using adaptive calibration of the vestibulo–ocular reflex (VOR) have indicated plasticity in both cerebellar cortex and the brainstem. To resolve this long-standing conflict, we attempted to identify the computational role of the brainstem site, by using an adaptive filter version of the cerebellar microcircuit to model VOR calibration for changes in the oculomotor plant. With only cortical plasticity, introducing a realistic delay in the retinal-slip error signal of 100 ms prevented learning at frequencies higher than 2.5 Hz, although the VOR itself is accurate up to at least 25 Hz. However, the introduction of an additional brainstem site of plasticity, driven by the correlation between cerebellar and vestibular inputs, overcame the 2.5 Hz limitation and allowed learning of accurate high-frequency gains. This “cortex-first” learning mechanism is consistent with a wide variety of evidence concerning the role of the flocculus in VOR calibration, and complements rather than replaces the previously proposed “brainstem-first” mechanism that operates when ocular tracking mechanisms are effective. These results (i) describe a process whereby information originally learnt in one area of the brain (cerebellar cortex) can be transferred and expressed in another (brainstem), and (ii) indicate for the first time why a brainstem site of plasticity is actually required by Marr-Albus type models when high-frequency gains must be learned in the presence of error delay.     

Selection in favor of lysosomal storage disorders?

Four examples of Israeli communities or large families in which high consanguinity is common are presented, with two different lysosomal storage disorders within each community. In each of the four cases the stored substances share common chemical structure, despite the different lysosomal hydrolases involved in each disease. A similar phenomenon is known among the Ashkenazi Jews, in whom four of the most frequent hereditary disorders are lysosomal storage disorders, which are characterized by storage of sphingolipid derivatives. Similar findings are reported in the literature in other communities. We suggest that this phenomenon indicates a selection in favor of lysosomal storage disorders of similar nature in certain populations. The selection forces leading to this phenomenon have not been identified yet, and it has not yet been determined whether these forces are the same in the different communities presented here.     

Pervasive Natural Selection in the Drosophila Genome?

Over the past four decades, the predominant view of molecular evolution saw little connection between natural selection and genome evolution, assuming that the functionally constrained fraction of the genome is relatively small and that adaptation is sufficiently infrequent to play little role in shaping patterns of variation within and even between species. Recent evidence from Drosophila, reviewed here, suggests that this view may be invalid. Analyses of genetic variation within and between species reveal that much of the Drosophila genome is under purifying selection, and thus of functional importance, and that a large fraction of coding and noncoding differences between species are adaptive. The findings further indicate that, in Drosophila, adaptations may be both common and strong enough that the fate of neutral mutations depends on their chance linkage to adaptive mutations as much as on the vagaries of genetic drift. The emerging evidence has implications for a wide variety of fields, from conservation genetics to bioinformatics, and presents challenges to modelers and experimentalists alike.     

Does Learning or Instinct Shape Habitat Selection?

Habitat selection is an important behavioural process widely studied for its population-level effects. Models of habitat selection are, however, often fit without a mechanistic consideration. Here, we investigated whether patterns in habitat selection result from instinct or learning for a population of grizzly bears (Ursus arctos) in Alberta, Canada. We found that habitat selection and relatedness were positively correlated in female bears during the fall season, with a trend in the spring, but not during any season for males. This suggests that habitat selection is a learned behaviour because males do not participate in parental care: a genetically predetermined behaviour (instinct) would have resulted in habitat selection and relatedness correlations for both sexes. Geographic distance and home range overlap among animals did not alter correlations indicating that dispersal and spatial autocorrelation had little effect on the observed trends. These results suggest that habitat selection in grizzly bears are partly learned from their mothers, which could have implications for the translocation of wildlife to novel environments.