Comparative proteomics reveal characteristics of life-history transitions in a social insect

Wolschin, Florian; Amdam, Gro V.

doi:10.1186/1477-5956-5-10

Cited by 58 publications

(55 citation statements)

References 81 publications

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“…Hence, these data do not indicate that severe 'wear and tear' effects in the antennae of foragers would contribute to declined learning performance. Rather, declined learning performance could be due to changes in the central brain, as shown earlier for synaptic protein levels (Wolschin et al, 2009). Further, the performance decline 14days after foraging was initiated in the flight room (Fig.2) is in accord with previous work on bees under natural summer conditions (Behrends et al, 2007;Scheiner and Amdam, 2009;Tolfsen et al, 2011).…”

Section: Discussionsupporting

confidence: 88%

“…To this end we contrasted old worker types in post-winter colonies that were made broodless with reference groups in brood-right colonies ( Fig.3; see Experiment 3 in Materials and methods). While after 14days of foraging the vast majority of foragers typically dies (Dukas, 2008;Wolschin et al, 2009), we did not observe such decrease in old foragers of broodless hives. Similarly, we did not observe a pronounced increase of poor-learning individuals 14days after foraging was first confirmed for these individuals in the broodless colonies (data not shown).…”

Section: Experiments 3 -The Effect Of Brood Rearing On Behavioral Senecontrasting

confidence: 88%

“…In accord, by using mass spectrometry and quantitative anatomy, we recently demonstrated that the protein and synapse matrices of the calyx were not changed in aging summer foragers. This is despite protein level changes detected for other areas of the central brain (Wolschin et al, 2009), and the behavioral decline typical for this worker caste (Behrends et al, 2007;Dukas, 2008;. Cumulative evidence therefore suggests that the calyx, a major learning center, might show structural and molecular exceptions from accelerated aging patterns that are observed in other brain regions.…”

Section: Discussionmentioning

confidence: 76%

“…Further studies focused on systems including metabolism, as well as insulin signaling, and identified age-related abundance changes for molecules involved in neuronal signaling and growth (Ament et al, 2008;Roberts and Elekonich, 2005;Wolschin and Amdam, 2007;Wolschin et al, 2009). In contrast, little is known about biomarkers of cellular senescence, which often can provide a more direct indication of deterioration than protein expression (Hsieh and Hsu, 2011;Seehuus et al, 2006a;Tolfsen et al, 2011).…”

Section: Introductionmentioning

confidence: 99%

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Aging and its modulation in a long-lived worker caste of the honey bee

Münch

Kreibich

Amdam

2013

Journal of Experimental Biology

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SUMMARYHighly social animals provide alternative aging models in which vastly different lifespan patterns are flexible, and linked to social caste. Research in these species aims to reveal how environment, including social cues, can shape the transition between shortlived and extremely long-lived phenotypes with negligible senescence. Among honey bee workers, short to intermediate lifespans are typical for summer castes, while the winter caste can live up to 10 times longer. For summer castes, experimental interventions could predictably accelerate, slow or revert functional senescence. In contrast, little is known about the particular conditions under which periods of negligible senescence in winter castes can be disrupted or sustained. We asked how manipulation of social environment in colonies with long-lived winter bees might alter the pace of functional senescence, measured as learning performance, as well as of cellular senescence, measured as lipofuscin accumulation. We show that behavioral senescence becomes rapidly detectable when the winter state is disrupted, and changes in social task behaviors and social environment (brood) are induced. Likewise, we found that cellular senescence was induced by such social intervention. However, cellular senescence showed marked regional differences, suggesting that particular brain regions age slower than others. Finally, by preventing post-winter colonies from brood rearing, behavioral senescence became undetectable, even after transition to the usually short-lived phenotypes had occurred. We envision that social regulation of negligible functional senescence and highly dynamic accumulation of a universal symptom of cellular aging (lipofuscin) offers rewarding perspectives to target proximate mechanisms of slowed aging. Supplementary material available online at

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Section: Discussionsupporting

confidence: 88%

Section: Experiments 3 -The Effect Of Brood Rearing On Behavioral Senecontrasting

confidence: 88%

Section: Discussionmentioning

confidence: 76%

Section: Introductionmentioning

confidence: 99%

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Aging and its modulation in a long-lived worker caste of the honey bee

Münch

Kreibich

Amdam

2013

Journal of Experimental Biology

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“…days of foraging labour) to brain ageing. Yet because the transition from nest tasks to foraging is not only behavioural, but also associated with changes in brain gene and protein expression (Whitfield et al, 2003;Garcia et al, 2009), general metabolism (Crailsheim, 1986;Harrison, 1986;Toth and Robinson, 2005;Wolschin and Amdam, 2007a) and cell-based innate immunity (Amdam et al, 2005), it is unclear whether the connection is conferred by flight activity per se or whether it emerges because of other factors inherent to forager physiology.…”

Section: Introductionmentioning

confidence: 99%

Flight restriction prevents associative learning deficits but not changes in brain protein-adduct formation during honeybee ageing

Tolfsen

Baker

Kreibich

et al. 2011

Journal of Experimental Biology

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SUMMARYHoneybees (Apis mellifera) senesce within 2weeks after they discontinue nest tasks in favour of foraging. Foraging involves metabolically demanding flight, which in houseflies (Musca domestica) and fruit flies (Drosophila melanogaster) is associated with markers of ageing such as increased mortality and accumulation of oxidative damage. The role of flight in honeybee ageing is incompletely understood. We assessed relationships between honeybee flight activity and ageing by simulating rain that confined foragers to their colonies most of the day. After 15days on average, flight-restricted foragers were compared with bees with normal (free) flight: one group that foraged for ~15days and two additional control groups, for flight duration and chronological age, that foraged for ~5days. Free flight over 15days on average resulted in impaired associative learning ability. In contrast, flight-restricted foragers did as well in learning as bees that foraged for 5days on average. This negative effect of flight activity was not influenced by chronological age or gustatory responsiveness, a measure of the bees' motivation to learn. Contrasting their intact learning ability, flight-restricted bees accrued the most oxidative brain damage as indicated by malondialdehyde protein adduct levels in crude cytosolic fractions. Concentrations of mono-and poly-ubiquitinated brain proteins were equal between the groups, whereas differences in total protein amounts suggested changes in brain protein metabolism connected to forager age, but not flight. We propose that intense flight is causal to brain deficits in aged bees, and that oxidative protein damage is unlikely to be the underlying mechanism.Supplementary material available online at

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Queen Honeybee and Me: Forever Young? Conserved Pathways for Longevity

Knäblein

Huber

2013

Modern Biopharmaceuticals

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Comparative proteomics reveal characteristics of life-history transitions in a social insect

Cited by 58 publications

References 81 publications

Aging and its modulation in a long-lived worker caste of the honey bee

Aging and its modulation in a long-lived worker caste of the honey bee

Flight restriction prevents associative learning deficits but not changes in brain protein-adduct formation during honeybee ageing

Queen Honeybee and Me: Forever Young? Conserved Pathways for Longevity

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