. Antimicrobial peptides are host-encoded immune effectors that combat pathogens and shape the microbiome in plants and animals. However, little is known about how the host antimicrobial peptide repertoire is adapted to its microbiome. Here, we characterized the function and evolution of the
. Diptericin
. antimicrobial peptide family of Diptera. Using mutations affecting the two
. Diptericins
. (
. Dpt
. ) of
. Drosophila melanogaster
. we reveal the specific role of
. DptA
. for the pathogen
. Providencia rettgeri
. and
. DptB
. for the gut mutualist
. Acetobacter
. The presence of
. DptA-
. or
. DptB-
. like genes across Diptera correlates with the presence of
. Providencia
. and
. Acetobacter
. in their environment. Moreover,
. DptA-
. and
. DptB-
. like sequences predict host resistance against infection by these bacteria across the genus
. Drosophila
. Our study explains the evolutionary logic behind the bursts of rapid evolution of an antimicrobial peptide family and reveals how the host immune repertoire adapts to changing microbial environments.
.

Scientists are increasingly overwhelmed by the volume of articles being
published. Total articles indexed in Scopus and Web of Science have grown
exponentially in recent years; in 2022 the article total was 47% higher than in
2016, which has outpaced the limited growth, if any, in the number of
practising scientists. Thus, publication workload per scientist (writing,
reviewing, editing) has increased dramatically. We define this problem as the
strain on scientific publishing. To analyse this strain, we present five
data-driven metrics showing publisher growth, processing times, and citation
behaviours. We draw these data from web scrapes, requests for data from
publishers, and material that is freely available through publisher websites.
Our findings are based on millions of papers produced by leading academic
publishers. We find specific groups have disproportionately grown in their
articles published per year, contributing to this strain. Some publishers
enabled this growth by adopting a strategy of hosting special issues, which
publish articles with reduced turnaround times. Given pressures on researchers
to publish or perish to be competitive for funding applications, this strain
was likely amplified by these offers to publish more articles. We also observed
widespread year-over-year inflation of journal impact factors coinciding with
this strain, which risks confusing quality signals. Such exponential growth
cannot be sustained. The metrics we define here should enable this evolving
conversation to reach actionable solutions to address the strain on scientific
publishing.

This study advances current knowledge in the field of host-microbe interactions by demonstrating that the two families of immune effectors, antimicrobial peptides and lysozymes, actively regulate the gut microbiota composition and abundance. Consequences of the loss of these antimicrobial peptides and lysozymes are exacerbated during aging, and their loss contributes to increased microbiota abundance and shifted composition in old flies.

AbstractAntimicrobial peptides (AMPs) are host-encoded antibiotics that combat invading pathogens. These genes commonly encode multiple products as post-translationally cleaved polypeptides. Recent studies have highlighted roles for AMPs in neurological contexts suggesting functions for these defence molecules beyond infection. During our immune study characterizing the antimicrobial peptide gene Baramicin, we recovered multiple Baramicin paralogs in Drosophila melanogaster and other species, united by their N-terminal IM24 domain. Not all paralogs were immune-induced. Here, through careful dissection of the Baramicin family’s evolutionary history, we find that these non-immune paralogs result from repeated events of duplication and subsequent truncation of the coding sequence from an immune-inducible ancestor. These truncations leave only the IM24 domain as the prominent gene product. Surprisingly, using mutation and targeted gene silencing we demonstrate that two such genes are adapted for function in neural contexts in D. melanogaster. We also show enrichment in the head for independent Baramicin genes in other species. The Baramicin evolutionary history reveals that the IM24 Baramicin domain is not strictly useful in an immune context. We thus provide a case study for how an AMP-encoding gene might play dual roles in both immune and non-immune processes via its multiple peptide products. We reflect on these findings to highlight a blind spot in the way researchers approach AMP research in in vivo contexts.Significance statementAntimicrobial peptides are immune proteins recently implicated in neurological roles. To date little attention has been paid to the contributions of different gene products in this function. Here we show that an antimicrobial peptide gene encodes multiple products with either immune-specific or neurological roles.

AbstractStaurozoa is an intriguing lineage of cnidarians bearing both polypoid and medusoid characters in the adult body plan. Miranda et al. (2016) provided a massive descriptive effort of specimen collection, sequencing, and character evolution. We also recently described the neuromusculature of two staurozoan species: Manania handi and Haliclystus “sanjuanensis.” We found that our M. handi samples genetically matched Manania gwilliami samples used in Miranda et al. (2016). Taking advantage of newly-deposited M. gwilliami sequence data, we confirm the identity of our M. handi samples, and provide additional sequence data for M. handi and H. sanjuanensis for future staurozoan identification efforts.

AbstractSelfish genes that bias their own transmission during meiosis can spread rapidly in populations, even if they contribute negatively to the fitness of their host. Driving X chromosomes provide a clear example of this type of selfish propagation. These chromosomes have important evolutionary and ecological consequences, and can be found in a broad range of taxa including plants, mammals and insects. Here, we report a new case of X chromosome drive (X drive) in a widespread woodland fly, Drosophila testacea. We show that males carrying the driving X (SR males) sire 80–100% female offspring and possess a diagnostic X chromosome haplotype that is perfectly associated with the sex ratio distortion phenotype. We find that the majority of sons produced by SR males are sterile and appear to lack a Y chromosome, suggesting that meiotic defects involving the Y chromosome may underlie X drive in this species. Abnormalities in sperm cysts of SR males reflect that some spermatids are failing to develop properly, confirming that drive is acting during gametogenesis. By screening wild‐caught flies using progeny sex ratios and a diagnostic marker, we demonstrate that the driving X is present in wild populations at a frequency of ~ 10% and that suppressors of drive are segregating in the same population. The testacea species group appears to be a hot spot for X drive, and D. testacea is a promising model to compare driving X chromosomes in closely related species, some of which may even be younger than the chromosomes themselves.