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The Major Histocompatibility Complex (MHC) genes encode proteins that initiate the adaptive immune response by presenting pathogen‐derived antigenic peptides to T lymphocytes. Host–pathogen coevolution drives MHC polymorphism, introducing intraspecific variation in host life expectancy. This variation interacts with optimal growth strategy, as growth increases reproductive potential. While mortality rate and body size‐dependent fecundity are major factors shaping life histories, the effect of intraspecific variation in MHC‐based immunity on the evolution of growth strategies and host body size remains unknown.Here, we model how host MHC–pathogen coevolution—and its concomitant impact on host mortality—can affect the evolution of host life histories, as represented by age at maturation and body size. Life histories were compared in scenarios with and without adaptive immune response under equal population‐level mortality rates.We show that host–pathogen coevolutionary dynamics selects for postponed maturation and increased body size. Although MHC genes and genes that determine body size were physically unlinked, selection imposed by the Red Queen process generated linkage disequilibrium between immunocompetent MHC alleles and the maturation‐postponing alleles that prolong growth phase and increase body size. Particularly large body size was attained when pathogens mutated slowly, thus allowing the advantage of resistant MHC alleles to persist over multiple generations.The emergence of adaptive immunity, which is pathogen‐specific and enables immunological memory, is considered a major evolutionary innovation of vertebrates. Our work suggests that the adaptive immune response, mediated by polymorphic MHC genes, may drive the evolution of host body size. This form of adaptive immunity may have thus predisposed vertebrates to evolve large body size and exhibit the macroevolutionary patterns of increasing body size over time that have been detected in comparative studies. Read the free Plain Language Summary for this article on the Journal blog. [ABSTRACT FROM AUTHOR]

Due to climate change, the timing of spring arrival and nesting onset in many migratory bird species have advanced. Earlier spring onsets prolong the available breeding period but can also deteriorate local conditions, leading to increased temporal variation in resource availability. This interaction between phenological shifts in nesting onset and short‐term temporal variation in food gain has unknown consequences for fitness of migratory bird species. We model two contrasting breeding strategies to investigate the fitness consequences of stochastically fluctuating food gain and storing of energetic reserves for reproduction. The model was inspired by the biology of common eiders (Somateria mollissima), which store extensive reserves prior to egg laying and incubation (capital breeding strategy), and king eiders (S. spectabilis), which continue to forage during nesting (income breeding strategy). For capital breeders, foraging prior to breeding increases energy reserves and clutch size, but for both strategies, postponing nesting reduces the chances of recruitment. We found that in scenarios with early spring onset, the average number of recruits produced by capital breeders was higher under conditions of stochastic rather than deterministic food gain. This is because under highly variable daily food gain, individuals successful in obtaining food can produce large clutches early in the season. However, income breeders do not build up reserve buffers; consequently, their fitness is always reduced, when food availability fluctuates. For both modeled strategies, resource uncertainty had only a minor effect on the timing of nesting onset. Our work shows that the fitness consequences of global changes in breeding season onset depend on the level of uncertainty in food intake and the degree to which reserves are used to fuel the reproductive effort. We predict that among migratory bird species producing one clutch per year, capital breeders are more resilient to climate‐induced changes in spring phenology than income breeders. [ABSTRACT FROM AUTHOR]

Abstract: The theory of life‐history evolution investigates how growth‐reproduction trade‐offs drive evolution of body size in uni‐ and multivoltine (one or more generations per year) arthropods. Existing theory does not predict how the length of the feeding season (season length hereafter) affects body size in semivoltine (i.e., juvenile period longer than 1 year) determinate growers and usually ignores that uni‐ and semivoltine arthropods accumulate large reserves to cover costs of diapause and future reproduction. Here, we present how the trade‐offs between growth, storage and reproduction drive evolution of body mass and reproductive strategy in arthropods with determinate growth. Our life‐history model concerns high‐latitude marine copepods living in a strongly seasonal environment. We find that small changes in season length and mortality rate translate into abrupt shifts in lean body mass (a proxy for body size). Body size shifts are caused by a change from multi‐ to uni‐ and semivoltine life cycles with semivoltine life histories selected for in short seasons and only if background mortality is low. Shifts in the number of generations per year do not translate into shifts in the mass of lipid reserves. The model predicts less reserves the shorter the winter. Season length alone is not a sufficient predictor of the degree of capital breeding. Storing for reproduction is strongly selected for under short season but low mortality rate. Hence, capital breeding contributes to fitness in uni‐ and semivoltine organisms whereas multivoltines are income breeders. We also show that storing reserves for diapause and capital breeding trades off with adult size of determinately growing arthropods. Our results, in particular regarding optimal body size, reproductive strategy (income‐to‐capital breeding) and degree of storage are relevant to a number of determinate growers, including insects and crustaceans. A plain language summary is available for this article. [ABSTRACT FROM AUTHOR]

Major histocompatibility complex (MHC) genes (referred to as human leukocyte antigen or HLA in humans) are a key component of vertebrate immune systems, coding for proteins which present antigens to T‐cells. These genes are outstanding in their degree of polymorphism, with important consequences for human and animal health. The polymorphism is thought to arise from selection pressures imposed by pathogens on MHC allomorphs, which differ in their antigen‐binding capacity. However, the existing theory has not considered MHC selection in relation to the formation of immune memory. In this paper, we argue that this omission limits our understanding of the evolution of MHC polymorphism and its role in disease. We review recent evidence that has emerged from the massive research effort related to the SARS‐CoV‐2 pandemics, and which provides new evidence for the role of MHC in shaping immune memory. We then discuss why the inclusion of immune memory within the existing theory may have non‐trivial consequence for our understanding of the evolution of MHC polymorphism. Finally, we will argue that neglecting immune memory hinders our interpretation of empirical findings, and postulate that future studies focusing on pathogen‐driven MHC selection would benefit from stratifying the available data according to the history of infection (and vaccination, if relevant). [ABSTRACT FROM AUTHOR]

Thiamin is an essential water‐soluble B vitamin known for its wide range of metabolic functions and antioxidant properties. Over the past decades, reproductive failures induced by thiamin deficiency have been observed in several salmonid species worldwide, but it is unclear why this micronutrient deficiency arises. Few studies have compared thiamin concentrations in systems of salmonid populations with or without documented thiamin deficiency. Moreover, it is not well known whether and how thiamin concentration changes during the marine feeding phase and the spawning migration. Therefore, samples of Atlantic salmon (Salmo salar) were collected when actively feeding in the open Baltic Sea, after the sea migration to natal rivers, after river migration, and during the spawning period. To compare populations of Baltic salmon with systems without documented thiamin deficiency, a population of landlocked salmon located in Lake Vänern (Sweden) was sampled as well as salmon from Norwegian rivers draining into the North Atlantic Ocean. Results showed the highest mean thiamin concentrations in Lake Vänern salmon, followed by North Atlantic, and the lowest in Baltic populations. Therefore, salmon in the Baltic Sea seem to be consistently more constrained by thiamin than those in other systems. Condition factor and body length had little to no effect on thiamin concentrations in all systems, suggesting that there is no relation between the body condition of salmon and thiamin deficiency. In our large spatiotemporal comparison of salmon populations, thiamin concentrations declined toward spawning in all studied systems, suggesting that the reduction in thiamin concentration arises as a natural consequence of starvation rather than to be related to thiamin deficiency in the system. These results suggest that factors affecting accumulation during the marine feeding phase are key for understanding the thiamin deficiency in salmonids. [ABSTRACT FROM AUTHOR]

In many annual plants, mollusks, crustaceans and ectothermic vertebrates, growth accompanies reproduction. The growth curves of these organisms often exhibit a complex shape, with episodic cessations or accelerations of growth occurring long after maturation. The mixed allocation to growth and reproduction has poorly understood adaptive consequences, and the life‐history theory does not explain if complex growth in short‐lived organisms can be adaptive.We model the trade‐off between growth and reproduction in a short‐lived organism evolving in a metapopulation. Individuals occupy risky or safe sites throughout their lives, but are uncertain regarding the risk of death. Modelled organisms are allowed to grow and produce offspring at specified time points (moults), although we also consider scenarios that approximate continuous growth and reproduction.Certain combinations of risky to safe sites select for strategies with mixed allocation to growth and reproduction that bet‐hedge offspring production in safe and risky sites. Our model shows that spatially heterogeneous environments select for mixed allocation only if safe sites do not become the prevailing source of recruits, for example, when risky sites are frequent. In certain conditions, growth curves are multi‐phasic, with allocation to growth that stops, remains constant or accelerates during adult life. The resulting complex growth curves are more likely to evolve in short‐lived organisms that moult several times per adult life.Our work shows that spatial heterogeneity can select for growth that accompanies reproduction and provides insights into the adaptive significance of complex growth curves. Short‐lived crustaceans are particularly predisposed to exhibit complex growth patterns as an adaptive response to spatially heterogeneous environments. Our results suggest that standard statistical growth models assuming adult growth rate to only decelerate over life are not well suited to approximate growth curves of short‐lived crustaceans. A free Plain Language Summary can be found within the Supporting Information of this article. [ABSTRACT FROM AUTHOR]

Accurate genotyping of complex systems, such as the major histocompatibility complex (MHC) often requires simultaneous analysis of multiple co-amplifying loci. Here we explore the utility of the massively parallel 454 sequencing method as a universal tool for genotyping complex MHC systems in nonmodel vertebrates. The power of this approach stems from the use of tagged polymerase chain reaction (PCR) primers to identify individual amplicons which can be simultaneously sequenced to the arbitrarily chosen coverage. However, the error-prone sequencing technology poses considerable challenges as it may be difficult to discriminate between sequencing errors and true rare alleles; due to complex nature of artefacts and errors, efficient quality control is required. Nevertheless, our study demonstrates the parallel 454 sequencing can be an efficient genotyping platform for MHC and provides an alternative to classical genotyping methods. We introduced procedures to identify the threshold that can be used to reduce number of genotyping errors by eliminating most of artefactual alleles (AA) representing PCR or sequencing errors. Our procedures are based on two expectations: first, that AA should be relatively rare, both overall and on per-individual basis, and second, that most AA result from errors introduced to sequences of true alleles. In our data set, alleles with an average per-individual frequency below 3% most likely represented artefacts. This threshold will vary in other applications according to the complexity of the genotyped system. We strongly suggest direct assessment of genotyping error in every experiment by running a fraction of duplicates: individuals amplified in independent PCRs. [ABSTRACT FROM AUTHOR]