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Brood parasitism involves the exploitation of host parental care rather than the extraction of resources directly from hosts. We identify defining characteristics of this strategy and consider its position along continua with adjacent behaviors but focus on canonical brood parasites, where parasitism is obligate and hosts are noneusocial (thereby distinguishing from social parasitism). A systematic literature survey revealed 59 independently derived brood parasitic lineages with most origins (49) in insects, particularly among bees and wasps, and other origins in birds (seven) and fish (three). Insects account for more than 98% of brood parasitic species, with much of that diversity reflecting ancient (≥100-million-year-old) brood parasitic lineages. Brood parasites usually, but not always, evolve from forms that show parental care. In insects, brood parasitism often first evolves through exploitation of a closely related species, following Emery's rule, but this is less typical in birds, which we discuss. We conducted lineage-level comparisons between brood parasitic clades and their sister groups, finding mixed results but an overall neutral to negative effect of brood parasitism on species richness and diversification. Our review of brood parasites reveals many unanswered questions requiring new research, including further modeling of the coevolutionary dynamics of brood parasites and their hosts. [ABSTRACT FROM AUTHOR]

[Display omitted] • Ultraconserved element phylogeny of the small carpenter bees, genus Ceratina, including nearly all known subgenera. • Ceratina originated in Africa ∼ 42 Ma, quickly reaching Palearctic and Indomalaya. • Biogeographic reconstruction shows single dispersal event to Americas 22 Ma. • Tropical areas are important in explaining present and historical Ceratina diversity. Small carpenter bees in the genus Ceratina are behaviourally diverse, species-rich, and cosmopolitan, with over 370 species and a range including all continents except Antarctica. Here, we present the first comprehensive phylogeny of the genus based on ultraconserved element (UCE) phylogenomic data, covering a total of 185 ingroup specimens representing 22 of the 25 current subgenera. Our results support most recognized subgenera as natural groups, but we also highlight several groups in need of taxonomic revision – particularly the nominate subgenus Ceratina sensu stricto – and several clades that likely need to be described as new subgenera. In addition to phylogeny, we explore the evolutionary history of Ceratina through divergence time estimation and biogeographic reconstruction. Our findings suggest that Ceratinini split from its sister tribe Allodapini about 72 million years ago. The common ancestor of Ceratina emerged in the Afrotropical realm approximately 42 million years ago, near the Middle Eocene Climatic Optimum. Multiple subsequent dispersal events led to the present cosmopolitan distribution of Ceratina , with the majority of transitions occurring between the Afrotropics, Indomalaya, and the Palearctic. Additional movements also led to the arrival of Ceratina in Madagascar, Australasia, and a single colonization of the Americas. Dispersal events were asymmetrical overall, with temperate regions primarily acting as destinations for migrations from tropical source regions. [ABSTRACT FROM AUTHOR]

Brood parasites represent a substantial but often poorly studied fraction of the wider diversity of bees. Brood parasitic bees complete their life cycles by infiltrating the nests of solitary host bees thereby enabling their offspring to exploit the food provisions intended for the host's offspring. Here, we present the draft assembly of the bee Holcopasites calliopsidis, the first brood parasitic species to be the subject of detailed genomic analysis. Consistent with previous findings on the genomic signatures of parasitism more broadly, we find that H. calliopsidis has the smallest genome currently known among bees (179 Mb). This small genome does not appear to be the result of purging of repetitive DNA, with some indications of novel repetitive elements which may show signs of recent expansion. Nor does H. calliopsidis demonstrate any apparent net loss of genic content in comparison with nonparasitic species, though many individual gene families do show significant contractions. Although the basis of the small genome size of this species remains unclear, the identification of over 12,000 putative genes--with functional annotation for nearly 10,000 of these--is an important step in investigating the genomic basis of brood parasitism and provides a valuable dataset to be compared against new genomes that remain to be sequenced. [ABSTRACT FROM AUTHOR]

[Display omitted] • UCEs allow taxon-rich and genome-wide phylogenetic study of brood parasitic Apidae. • An expanded concept of Nomadinae includes almost all parasitic apids. • Paraphyletic Osirini split into three tribes, including newly described Parepeolini. • Trend towards increasingly unrelated and diverse hosts over time. • Early nomadines parasitized related taxa before expanding diversity of hosts. Brood parasites (also known as cleptoparasites) represent a substantial fraction of global bee diversity. Rather than constructing their own nests, these species instead invade those of host bees to lay their eggs. Larvae then hatch and consume the food provisions intended for the host's offspring. While this life history strategy has evolved numerous times across the phylogeny of bees, the oldest and most speciose parasitic clade is the subfamily Nomadinae (Apidae). However, the phylogenetic relationships among brood parasitic apids both within and outside the Nomadinae have not been fully resolved. Here, we present new findings on the phylogeny of this diverse group of brood parasites based on ultraconserved element (UCE) sequence data and extensive taxon sampling with 114 nomadine species representing all tribes. We suggest a broader definition of the subfamily Nomadinae to describe a clade that includes almost all parasitic members of the family Apidae. The tribe Melectini forms the sister group to all other Nomadinae, while the remainder of the subfamily is composed of two sister clades: a "nomadine line" representing the former Nomadinae sensu stricto , and an "ericrocidine line" that unites several mostly Neotropical lineages. We find the tribe Osirini Handlirsch to be polyphyletic, and divide it into three lineages, including the newly described Parepeolini trib. nov. In addition to our taxonomic findings, we use our phylogeny to explore the evolution of different modes of parasitism, detecting two independent transitions from closed-cell to open-cell parasitism. Finally, we examine how nomadine host-parasite associations have evolved over time. In support of Emery's rule, which suggests close relationships between hosts and parasites, we confirm that the earliest nomadines were parasites of their close free-living relatives within the family Apidae, but that over time their host range broadened to include more distantly related hosts spanning the diversity of bees. This expanded breadth of host taxa may also be associated with the transition to open-cell parasitism. [ABSTRACT FROM AUTHOR]

The capacity to transition between distinct morphological forms is a key virulence trait for diverse fungal pathogens. A poignant example of a leading opportunistic fungal pathogen of humans for which an environmentally responsive developmental program underpins virulence is Candida albicans. C. albicans mutants that are defective in the transition between yeast and filamentous forms typically have reduced virulence. Although many positive regulators of C. albicans filamentation have been defined, there are fewer negative regulators that have been implicated in repression of filamentation in the absence of inducing cues. To discover novel negative regulators of filamentation, we screened a collection of 1,248 C. albicans homozygous transposon insertion mutants to identify those that were filamentous in the absence of inducing cues. We identified the Rho1 GAP Lrg1, which represses filamentous growth by stimulating Rho1 GTPase activity and converting Rho1 to its inactive, GDP-bound form. Deletion of LRG1 or introduction of a RHO1 mutation that locks Rho1 in constitutively active, GTP-bound state, leads to filamentation in the absence of inducing cues. Deletion of the Rho1 downstream effector PKC1 results in defective filamentation in response to diverse host-relevant inducing cues, including serum. We further established that Pkc1 is not required to sense filament-inducing cues, but its kinase activity is critical for the initiation of filamentous growth. Our genetic analyses revealed that Pkc1 regulates filamentation independent of the canonical MAP kinase cascade. Further, although Ras1 activation is not impaired in a pkc1Δ/pkc1Δ mutant, adenylyl cyclase activity is reduced, consistent with a model in which Pkc1 functions in parallel with Ras1 in regulating Cyr1 activation. Thus, our findings delineate a signaling pathway comprised of Lrg1, Rho1 and Pkc1 with a core role in C. albicans morphogenesis, and illuminate functional relationships that govern activation of a central transducer of signals that control environmental response and virulence programs. [ABSTRACT FROM AUTHOR]