Researchers used a forward genetic approach to identify genes that affect a social behavior in honey bees.

For more than 30 years, honey bee geneticist Robert E. Page, Jr. and his colleagues have sought the genes that influence a colony trait that only emerges from interactions between thousands of individual bees — a social phenotype.

Such traits are notoriously difficult to study. As hard as it is to disentangle a gene’s effect on behavior from environmental influences, these challenges are greatly multiplied by the complex interactions between genetically different individuals forming and altering their own social environments. As a result, mapping quantitative trait loci (QTLs) for social behavior long seemed out of reach. A recent paper published in GENETICS surveys the three decades of work that culminated in identifying genes that affect a complex, socially-regulated foraging behavior.

“Everything flowed from our observations of the behaviors that were associated with foraging behavior and division of labor and the resulting impact on the amount of pollen stored in the comb,” says Page, a researcher at Arizona State University. “Over time, we adapted new technologies to ask questions about those phenomena in different ways. By bringing together a host of different toolkits, we were able to build a story of the underlying genetic basis of a very complex social trait.”

Pollen hoarders

In a honey bee colony, some of the bees specialize in collecting pollen and hoarding this protein-rich food in wax cells near the “nursery” where eggs and larvae develop. Some of the bees eat the pollen and produce glandular secretions to feed the larvae; in turn, the larvae produce pheromones that stimulate foragers to collect pollen.

Despite the complexity of factors involved — thousands of individual bees, larvae, their interactions, and their environment — the total amount of pollen stored in the colony is a regulated trait. In a previous study, ASU reseacher Professor Jennifer established this by adding and removing pollen from honey bee colonies and observing the changes in foraging behavior. Each colony had a set level of stored pollen that the bees collectively sought to maintain; when researchers added pollen, foraging decreased until excess pollen had been consumed, and when researchers removed pollen, foraging increased until pollen again reached the colony’s standard level.

Using selective breeding, Page’s team generated strains of honey bees that substantially differ in amount of pollen stored within just three generations. “People have tried for decades to breed bees that store more honey, but honey storage is a very sloppily regulated trait,” says Page. “As long as nectar is available, bees will bring it back and stick it anywhere they can find space in the hive. In contrast, pollen storage offers excellent consistency of measurement.”

Phenotypic and genotypic analysis

Using a wide range of methods, Page and his colleagues studied the phenotypes and genotypes of these strains for 42 generations of selection. Phenotypic mapping revealed that bees in colonies that store more pollen are likely to have more ovarioles (the egg-producing structures in the insect ovary) and to be more sensitive to sugar than those from the colonies with less pollen. One research collaborator, Ying Wang, went so far as to painstakingly graft ovarioles from worker bees into recipients from a colony that produced less, which in turn affected the recipients’ behavior.

When they began to map genetic trait determination, the researchers expected that individual behavior would be more selectable than complex social traits playing out across large groups. Instead, they were surprised to find that genotype explained roughly 41 percent of colony variance in stored pollen but only two percent of individual variance in pollen collection.

Digging down to the genetic level, Page and his colleagues performed QTL mapping for the social phenotype of pollen hoarding along with individual foraging behavior, physiology, and anatomical traits. From the gene lists for each QTL they identified candidate genes of interest based on the phenotypic architecture and assessed them using expression assays and gene knockdown. Ultimately, they identified three genes of special interest, all of which have some association with ovary size. Future studies will involve examining the effects of these genes in developing larvae more closely.

A vertical approach

Page attributes his success in part to his tenacity in pursuing a “vertical approach”—interrogating a single question at every level of influence, starting with social interaction and working down to examine individual behavior, morphological differences, physiology, developmental processes, and genetic variation.

Pursuing this vertical approach over so many years involved the work of countless expert apiculturists, laboratory technicians, students, and fellow researchers alongside Page. “Our success came from combining the right people with the right tools as they became available,” he says. “Everyone who came through my lab made it better and brought something new.”

CITATION:
Societies to genes: can we get there from here?
Robert E Page, Jr.
GENETICS 2021; iyab104
https://doi.org/10.1093/genetics/iyab104

The gene Ade2 links metabolism and sleep in the fat bodies of Drosophila.

All animals need to eat and sleep. In fact, these critical behaviors are intertwined: animals adjust their sleep needs based on food availability and energy storage. In a Featured article in G3, Yurgel et al. delved into the molecular mechanisms that connect sleep and metabolism in the fruit fly.

A growing body of evidence suggests that the fat body, an adipose-like organ in Drosophila responsible for fat storage and detoxification, regulates complex behaviors—but little is known about its relationship to sleep. Somewhat analogous to the mammalian liver, the fat body secretes hormones that influence fly behaviors, much the same way that human organs like the pancreas and stomach secrete hormones that trigger hunger or satiation, which in turn drive you to eat—or not.

Because sleep and metabolism are so interconnected, the authors hypothesized that genes in the fat body that are associated with hunger might also play a role in regulating sleep. Using RNAi, they knocked down the expression of 113 genes previously reported to be upregulated in the fly fat body under conditions of starvation. They then measured how long these flies slept compared to controls.

The screen showed that decreasing fat body expression of  Ade2, a highly conserved purine biosynthesis gene, caused flies to sleep, on average, 200 minutes less than controls—a reduction of ~20%. Since homozygous mutations in Ade2 are lethal, the authors confirmed that flies with heterozygous mutations also sleep less than wild-type, phenocopying the knockdown results.

Expressing additional Ade2 in the fat bodies of mutant flies partially rescued the short sleep phenotype; however, overexpression of Ade2 in wild-type fly fat bodies had no effect on sleep. This suggests that Ade2 is needed for normal sleep, but additional Ade2 isn’t enough to increase that normal sleep duration.

Other behaviors, including walking activity and arousal threshold, are connected to sleep behaviors in the fly. Ade2-deficient flies showed no change in arousal threshold, but some mutants trended toward increased walking activity. The authors interpret this increased walking activity as similar to the hyperactivity observed in starving flies.

Analysis of energy stores revealed decreased levels of triglycerides and free glucose but normal levels of glycogen—consistent with a starvation state. Energy stores that mirror starvation are consistent with the hyperactivity observed in the walking activity assays, since that behavior is also seen in starving flies. These data led the authors to propose that Ade2 is required for normal storage of triglycerides and free glucose and that its loss puts the fly into a starvation-like state, which in turn promotes sleep.

Typically, genetic studies of behavior have focused on the nervous system, but this study highlights the importance of also considering non-neuronal factors like fat tissue, which may be significant pieces of the puzzle.

CITATION:

Ade2 Functions in the Drosophila Fat Body To Promote Sleep

Maria E. Yurgel, Kreesha D. Shah, Elizabeth B. Brown, Carter Burns, Ryan A. Bennick, Justin R. DiAngelo, Alex C. Keene

G3: Genes, Genomes, Genetics

November 2018 8: 3385-3395; https://doi.org/10.1534/g3.118.200554

http://www.g3journal.org/content/8/11/3385

Parent-of-origin effects help determine how lab rats respond to stress.

Although your father and mother each contribute a copy of your genes, these copies don’t always play equal roles. Instead, one parent’s gene can have a disproportionate effect on the offspring’s phenotype, resulting in complex patterns of inheritance. In G3: Genes|Genomes|Genetics, Mont et al. examined such effects in the behavior of lab rats.

One example of parent-of-origin effects (PoE) is genomic imprinting, a phenomenon in which only either the maternal or paternal allele of a gene is expressed. Imprinting is associated with a range of developmental and behavioral phenotypes in mammals, and disruption of certain imprinted genes can cause human diseases like Prader-Willi, Angelman, and Beckwith-Wiedemann syndromes.

Although a great deal of work has been done on PoE in mice, much less is understood in rats, which show more complex behaviors. Thus, the authors began their study with a broad assessment of 199 phenotypes in a large cross of rats for which parental information was available. To look for potential examples of PoE, they developed a way to separate out the portion of trait variance that was dependent on inheritance in the usual sense—where there is no difference between maternally and paternally inherited alleles—from that which contrasts the mother versus the father. The latter component can arise from several causes, including true PoE, maternal effects (i.e. gene expression in the mother that influenced offspring taits), paternal effects (the equivalent for the father), and environmental effects from sharing a cage with the mother and some of the siblings. If there were no PoE, then values for each parent would be equivalent; however, the authors found that they were different for 86% of the phenotypes assessed.

If imprinted loci are known to be rare, why are these PoE-related effects seemingly so pervasive? The rat results are consistent with experiments done in mice, which also found widespread PoE-like phenomena and suggested that these effects may be due in part to the indirect effects of imprinted loci—that is, the effects of imprinting can ripple through the genome to trigger many additional phenotypic consequences.

Of particular note, the authors found that coping behaviors—how the animals reacted to stress—showed some of the most significant differences between maternal and paternal contributions, which is suggestive of PoE. However, confounding variables, such as dominance, can also generate PoE, so further experimentation was required to confirm this finding.

To test for PoE related to coping behaviors, the authors crossed two rat strains: RHA and RLA. Stressed RHA rats tend to display active behaviors, such as fleeing, whereas RLA rats tend to be passive when stressed, either freezing or self-grooming. These behaviors were assessed in the offspring of reciprocal crosses using the elevated zero maze, in which rats are placed in a ring-shaped elevated platform with alternating open and walled sections. The rats are then observed for anxiety-like behaviors around the open sections, since rats prefer closed spaces when they are exploring a new environment. The behavior of offspring in the maze tended to fit the behavior profile of the maternal strain: rats with RHA mothers and RLA fathers exhibited more active behavior (matching their RHA mothers), and vice versa.

The authors suggest that these differences might be due to known differences in epigenetic modifications on neurotransmitter receptor genes in the two rat strains, although further research is needed to define the exact mechanism for this phenomenon.

CITATION:

Coping-Style Behavior Identified by a Survey of Parent-of-Origin Effects in the Rat

Carme Mont, Polinka Hernandez Pilego, Toni Cañete, Ignasi Oliveras, Cristóbal Río-Álamos, Gloria Blázquez, Regina López-Aumatell, Esther Martínez-Membrives, Adolf Tobeña, Jonathan Flint, Alberto Fernández-Teruel, Richard Mott

G3: Genes|Genomes|Genetics October 2018 8: 3283-3291;

http://www.g3journal.org/content/8/10/3283

https://doi.org/10.1534/g3.118.200489

A new collection of inbred flies provides a tool for studying genetic control of sleep.

Sleep is vital for a healthy life, but some of us seem to get by with less snoozing than others. This individual variation isn’t unique to humans; fruit flies also show a variety of sleep patterns. These differences could potentially reveal more than just which flies are consistent cat-nappers—understanding the genetic basis of sleep variation could help pinpoint some of the molecular mechanisms that govern this essential and evolutionarily conserved process. In G3: Genes|Genomes|Genetics, Serrano Negron et al. describe a collection of inbred fly lines with extreme sleep behaviors that will serve as a useful tool for exploring such questions.

In a previous study, the authors had worked with flies from the Drosophila Genetic Reference Panel (DGRP), which is a large panel of inbred lines derived from a natural population. They chose the five longest-sleeping and five shortest-sleeping DGRP lines and allowed them to cross at random for 21 generations to produce an outbred population. They then used artificial selection to produce two long-sleeping and two short-sleeping populations.

In the new report, the authors created inbred lines from these long-sleeping and short-sleeping populations. Creating inbred lines is useful for gene editing studies because it reduces experimental noise caused by background genetic variation. To create lines of flies that sleep for either a very long or very short time, they mated one male and one female from one of the selected populations and then selected one male and one female from the progeny to propagate the line. They repeated this for 20 generations, eventually creating 39 inbred lines (19 long-sleeping lines and 20 short-sleeping lines), which were termed the Sleep Inbred Panel.

The duration of night sleep in the inbred lines ranged from just over an hour to nearly 11.5 hours, confirming that the extremes of the phenotypes had been maintained in the lines. The phenotypes were comparable to the selected parental populations, showing that the inbreeding process reduced genetic variability without drastically altering the sleep patterns. Interestingly, most of the variation between the new panel and the parental populations was due to short-sleeping inbred flies sleeping a little more than parental flies, which is likely because short sleep times made the flies less fit. Individual short-sleeping flies also showed more variation in how much they slept, likely for similar reasons.

By sequencing the genomes of flies in the panel, the authors identified a number of SNPs and other genomic variations associated with the sleep phenotypes, and they traced many of these variations back to the original DGRP lines. This resource can now be used to study the genetic underpinnings of sleep and may one day help shed light not only on ordinary differences between night owls and early birds but also on the causes of devastating sleep disorders.

Citation:

The Sleep Inbred Panel, a Collection of Inbred Drosophila melanogaster with Extreme Long and Short Sleep Duration

Yazmin L. Serrano Negron, Nancy F. Hansen, Susan T. Harbison

G3: Genes, Genomes, Genetics September 2018 8: 2865-2873;

https://doi.org/10.1534/g3.118.200503

http://www.g3journal.org/content/8/9/2865

Food-deprivation inhibits the stress-induced sleep response in C. elegans.

For many animals, the essential physiological drives of sleep and food are intimately linked. You might have noticed this if you’ve ever stayed up far too late and found yourself craving a snack. Yet because it’s impossible for most animals to eat and sleep at the same time, these two biological necessities must compete with each other. In GENETICS, Goetting et al. report what happens when the need for sleep and the need for food come into direct conflict in the model nematode Caenorhabditis elegans.

When C. elegans is exposed to a stressful condition like high heat or UV radiation, it goes into a quiescent state called stress-induced sleep (SIS). Sleeping worms cease moving and feeding, and they barely respond to normally unpleasant stimuli—unless they are rudely awoken by a sharp poke.

In contrast, the authors found that food-deprived worms were less prone to this stress-induced snooze than their well-fed counterparts. This was true regardless of whether there was more food around to forage for; that is, the worms tended to remain active after stress whether or not they were provided with additional food after being starved.

The authors also found that starvation-induced sleep-suppression was enhanced when there were more worms on the plate. This makes sense, because higher population densities mean fewer resources, so seeking food instead of going to sleep is likely the better option. Interestingly, crowding only inhibited SIS when worms were starved; well-fed worms in crowded plates showed no change in SIS after stress treatment.

Insulin signaling and TGF-β signaling play major roles in sensing food availability in C. elegans, so the authors asked whether these pathways play a role in SIS under normal conditions. They found that worms with mutations in a TGF-β ligand, but not the insulin receptor, had impairments in SIS. Further investigation revealed that TGF-β involvement in SIS is downstream of the ALA neuron (a master neural regulator of SIS) and dependent on the gene DAF-3, which is involved in TGF-β signaling.

If this DAF-3-dependent pathway was necessary and sufficient for food-deprivation-induced inhibition of SIS, it would follow that worms lacking DAF-3 would have no trouble falling asleep after being starved and stressed—but when the authors tested this, they instead found that the DAF-3 mutants had the same response as wild-types: they stayed awake. Therefore, the authors conclude that although the TGF-β pathway plays a role in normal SIS, it is not solely responsible for the lack of SIS when worms are starved. Consistent with this notion, the authors uncovered evidence that the TOR signaling pathway, which is active when nutrients are available and promotes growth and protein synthesis, plays a role in starvation-induced sleep suppression as well.  

Since sleep deprivation can be deadly, the authors tested whether food deprivation affected how much the worms needed to sleep to stay alive. They found that worms that were deprived of food, stressed, and then kept awake survived better than worms that were just stressed and kept awake. Thus, starving the worms allowed them to stay awake, at least in part, because they needed their sleep less.

CITATION:

Food-Dependent Plasticity in Caenorhabditis elegans Stress-Induced Sleep Is Mediated by TOR–FOXA and TGF-b Signaling

Desiree L. Goetting, Rony Soto, Cheryl Van Buskirk

Genetics August 2018 209: 1183-1195; https://doi.org/10.1534/genetics.118.301204

Imprinted genes can have oppositional effects on adult behavior in mice.

Mammalian genomes show the marks of a genetic tug-of-war between mothers and fathers. These imprinted genes are marked by epigenetic modifications, which means the expression of an imprinted allele depends on whether it was inherited from the mother or the father. A new report in GENETICS expands our understanding of this phenomenon by describing a pair of imprinted genes with opposing effects on adult mouse behavior.

Seeking the evolutionary underpinnings of imprinting has fueled a number of theories and debates. One explanation is based on the conflicting evolutionary pressures on alleles with different parental origins. This theory of intragenomic conflict suggests that the function of imprinting is to control the expression of genes that have opposite effects on maternal and paternal fitness. For example, a paternally inherited allele might favor the growth of offspring as large as possible, but a gene inherited from the mother might instead favor conserving maternal resources for future offspring. Supporting this idea, a number of examples have been found where pairs of genes with antagonistic effects on embryonic growth and early development have inverse patterns of imprinting (i.e. one is expressed only from the paternal allele and the other only from the maternal allele).

In the mouse central nervous system, only the maternal copy of Nesp55 is expressed, while only the paternal copy of Grb10 is expressed. The authors of the GENETICS study previously found that mice lacking maternal Nesp55 make more impulsive choices, but the role of Grb10 was unknown. Given that the two genes have similar expression patterns, the authors hypothesized that they might play related roles.

To address this question, the authors used the same experimental setup they had used for their previous study of Nesp55. They tested mice lacking paternal Grb10 and their wild-type littermates with two different measures of impulsivity. First, they tested impulsive choice by using a delayed reinforcement test, in which mice have to choose between a small reward immediately or a larger reward after a wait. Then, they measured impulsive action by using a stop-signal reaction time test, where mice had to learn to stop a prepotent action in order to get a reward. Although “impulsive choice” and “impulsive action” are deceptively similar terms, they refer to discrete behaviors.

In their previous study, the authors found that mice lacking maternal Nesp55 make more impulsive choices, i.e. they show a preference for a small but quick reward. In this study, mice lacking paternal Grb10 showed the exact opposite phenotype; they made significantly fewer impulsive choices. The behavioral effect was quite specific; all the mice studied showed no change in impulsive action. This suggests that these two genes have opposing effects on this particular aspect of mouse behavior—and this behavior could be subject to conflicting selection pressures, in line with the theory of intragenomic conflict.

This is the first report of imprinted genes acting in opposition in adult behavior, and it suggests that the genomic tug-of-war between parental alleles could have effects that extend into adulthood—far beyond those observed in utero and in early development. The authors suggest that such imprinted genes may even play roles in human disorders that involve impulsivity, like addiction.

CITATION:

Impulsive Choice in Mice Lacking Paternal Expression of Grb10 Suggests Intragenomic Conflict in Behavior

Claire L. Dent, Trevor Humby, Katie Lewis, Andrew Ward, Reiner Fischer-Colbrie, Lawrence S. Wilkinson, Jon F. Wilkins, Anthony R. Isles

GENETICS May 1, 2018 vol. 209 no. 1 233-239; DOI: 10.1534/genetics.118.300898

http://www.genetics.org/content/209/1/233 

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A new study reveals genetic changes that affect social behavior in chickens.

We have a number of phrases that relate human behavior to that of chickens; for example, when you accuse someone of acting “chicken,” you’re likely calling them a coward. If someone is running around like a chicken with their head cut off, they’re probably frantic and disorganized. The reality of chicken behavior is, of course, more complex than these cliches; chickens naturally live in groups and exhibit many of the same social behaviors that other animals do, like anxiety and seeking out friends. Some chickens are more sociable than others, but what accounts for this difference? In a report published in GENETICS, Johnsson et al. analyzed the genes and behavior of chickens to find out.

The authors were specifically interested in social reinstatement (SR) in chickens. Social reinstatement measures how sociable a bird is; it is calculated by removing a chicken from its fellows and observing how long it takes to seek them out again. The authors performed this test on hundreds of chickens who were also genotyped with a SNP array. They identified correlations between genetic and phenotypic differences using quantitative trait locus analysis. The authors also analyzed gene expression in the chickens’ hypothalamuses—which play an important role in behavior and sociality—to bolster their findings.

A number of SNPs correlated with different social reinstatement scores. For example, differences in the gene TTRAP, which is associated with neurodegeneration and early-onset Parkinson’s disease, strongly correlated with differences in SR. Other neuron-associated genes, like PRDX4, also had correlations with SR—as were some genes that, until now, had never been associated with neurology or behavior.

These findings are correlative, and further research will be needed to prove a causal link between the identified genes and behavior. However, by identifying a list of candidate behavior-related genes, researchers have promising places to start looking for causal links, rather than running around like… well, you get it.

CITATION:

Genetics and Genomics of Social Behavior in a Chicken Model

Martin Johnsson, Rie Henriksen, Jesper Fogelholm, Andrey Höglund, Per Jensen, Dominic Wright

GENETICS Early online March 12, 2018; DOI: 10.1534/genetics.118.300810

http://www.genetics.org/content/early/2018/03/12/genetics.118.300810 

Whether it’s a battle over territory or a brawl over a sports game, aggressive behavior is a hallmark of the animal kingdom. The influence genetics has on aggression is undeniable—but the process of determining the genes involved has been frustratingly slow.

To better understand genetic factors involved in aggression, some researchers have turned to male fruit flies, which fight, if necessary, to obtain mates. The fruit fly is a good choice for these studies because flies are easy to grow and genetically manipulate. But there’s one major issue: in flies, as in other animals, it’s difficult and time-consuming to screen for aggression. The consequence is that most research on the genetics of aggression in flies has been focused on just a handful of genes that were already predicted to have an effect.

To cast a wider net, Davis et al. have devised a new method to quickly and easily screen for aggression. They noticed that groups of aggressive male flies housed together developed battle scars: wing damage that occurs when one fly grabs another’s wings midflight to destabilize its opponent. In some cases, the damage amounts to just a few nicks, but flies in severely aggressive groups sometimes sustain losses of large pieces of their wings.

Checking for wing damage can be done quickly, allowing the researchers to screen about 1400 mutant fly strains for aggression. Of those, they found that flies from only 41 strains had wing damage, and a deeper examination revealed that five of those strains were very aggressive. When the group sequenced the genome of a fly from one of the most aggressive strains, they found that it had a mutation in the gene Shaker, which encodes part of an ion channel involved in neuron function.

Shaker was not previously known to be involved with aggression, and this new technique has the potential to uncover many other such links between specific genes and aggressive behaviors. Pinning down these genes will not only help reveal how this complex behavior is controlled, it will provide candidate genes when an analysis like this one isn’t feasible, such as in studies of many other animals—including humans.

CITATION:

Davis, S.; Thomas, A.; Liu, L.; Campbell, I.; Dierick, H. Isolation of Aggressive Behavior Mutants in Drosophila Using a Screen for Wing Damage.
GENETICS, 208(1), 273-282.
DOI: 10.1534/genetics.117.300292
http://www.genetics.org/content/208/1/273

When you catch a nasty cold, curling up in bed to sleep may be the only activity you can manage. Sleeping in response to stress isn’t a uniquely human behavior: many other animals have the same reaction, and it’s not clear why. While the circadian sleep that follows the pattern of the clock has been studied extensively, sleep that’s triggered by stress is far less understood.

In the October issue of GENETICS, DeBardeleben et al. describe their investigation of stress-induced sleep in the nematode worm Caenorhabditis elegans, using ultraviolet C (UVC) radiation to induce stress. The researchers found that after UVC exposure, the worms initially wriggled more, but then their movements slowed as if they were dozing off.

To make sure the worms were truly asleep and not just resting quietly, DeBardeleben et al. exposed the worms to octanol vapor, which causes wakeful worms to immediately recoil because they find the chemical noxious. The UVC-treated worms took a moment to move away—a clue they were truly sleeping. The researchers also made sure the UVC-exposed worms weren’t just taking longer to react because they were injured by the light treatment. They tried waking a few of them by prodding them gently with a wire, and the worms that were poked reacted much more quickly to the foul octanol than those left undisturbed.

After the researchers established that UVC exposure caused stress-induced sleep in C. elegans, they investigated the genetic basis of the phenomenon. Since UV radiation damages DNA, they hypothesized that proteins involved in the response to DNA damage might be connected to the worms’ drowsiness. They found that mutating the gene for one of these proteins, CEP-1, reduced how sleepy the worms got after UVC irradiation.

CEP-1’s mammalian homolog is p53, a protein so critical in the response to DNA damage that it’s often called the guardian of the genome. Many mammals also respond to radiation with sleepiness; for example, radiation therapy for human cancers and some other diseases is associated with intense lethargy. The reason for the urge to sleep isn’t known for certain, but some research suggests it may actually be protective. Rabbits that sleep after an infection, for example, are more likely to survive than their wakeful counterparts.

DeBardeleben et al. suggest sleeping after stressful events helps the organism funnel more resources into cellular repair. Still, the restorative properties of sleep—stress-induced or otherwise—remain to be fully understood.

CITATION:

DeBardeleben, H.; Lopes, L.; Nesseland, M.; Raizen, D. Stress-Induced Sleep After Exposure to Ultraviolet Light Is Promoted by p53 in Caenorhabditis elegans.
GENETICS, 207(2), 571-582.
DOI: 10.1534/genetics.117.300070
http://www.genetics.org/content/207/2/571

A green, iridescent bee perches on a pink flower, extending its proboscis to reach the sweet nectar inside. He’s not just after a meal—he’s also collecting fragrant substances to store inside his hollow rear legs. Later, he’ll buzz his wings to release the aroma with the hope of attracting a mate. The cover of the September issue of G3 features a photograph of this eye-catching insect: a type of orchid bee called Euglossa dilemma. Orchid bees inhabit the neotropical realm, a region encompassing most of South America, some of Central America, and a tiny fraction of southern North America. There, these bees are some of the most important pollinators of flowering plants.

In the same issue of G3, Brand et al. report a draft assembly of the nuclear and mitochondrial genome of E. dilemma, the first draft genome of any species in the genus Euglossa. The genome revealed several interesting facts about the bees; for example, they have one of the largest genomes of any insect, loaded with repetitive sequences. Their assembly will also be a boon to bee researchers, from those seeking to know more about how to conserve these essential pollinators to those studying bee evolution.

Of particular interest is the evolution of one of many bees’ most fascinating traits: the ability to form intricate social structures. E. dilemma, unlike its close relatives the honeybee, stingless bee, and bumble bee, doesn’t actually live in communal hives. If the male orchid bee succeeds in seducing a female with his foraged scents, she’ll lay their eggs in a small nest of up to twenty cells, where she’ll feed the larvae nectar and pollen. Orchid bees may build their nests near each other, giving the impression of a loosely connected society, but groups of nests don’t form communities like hives. However, daughter bees sometimes stay in their mothers’ nests to help her raise a new generation—a type of social interaction that may have been one of the evolutionary stepping stones toward hives in insects like honeybees. Using the new genome as a starting point, researchers might be able to learn more about the evolution of this complex behavior, increasing our knowledge of many more types of these industrious insects.

CITATION:
Brand, P.; Saleh, N.; Pan, H.; Li, C.; Kapheim, K.; Ramírez, S. The Nuclear and Mitochondrial Genomes of the Facultatively Eusocial Orchid Bee Euglossa dilemma.
G3: Genes|Genomes|Genetics, 7(9), 2891-2898.
DOI: 10.1534/g3.117.043687
http://www.g3journal.org/content/7/9/2891