Molecular biology and evolution最新文献

Limbs exhibit adaptive differentiation along their dorsal-ventral (DV) axis, determined by the dorsal expression of the LIM homeobox gene Lmx1b. The paired appendages (ie the pectoral and pelvic fins from which limbs evolved) arose in an early jawless ancestor via co-option of a midline-fin genetic program including modules for anterior-posterior (AP) and proximal-distal (PD) patterning. Unlike the AP and PD axes, median fins lack an unambiguous DV axis, leaving the origin of this DV pattern in paired appendages unresolved. Here, we describe Lmx1b expression in the posterior midline fins of cichlids, sturgeons, catsharks, and lampreys, revealing an ancestral role for this gene predating the origin of paired appendages. In median fins, Lmx1b activation depends on shh from the ZPA, whereas in paired fins it relies on ectodermal wnt signaling, indicating the evolution of novel regulatory inputs for dorsal patterning. We observe that ephA4b, a putative Lmx1b target, is co-expressed with Lmx1b in dorsal pectoral and posterior midline fins and downregulated alongside Lmx1b, suggesting a role in both fin types related to axon guidance. We propose that novel regulation drove the repurposing of Lmx1b from posterior to dorsal fin determinant, with co-option of conserved downstream targets. Altogether, our findings demonstrate that the DV axis of paired appendages represents an evolutionary innovation arising from the integration of ancestral midline fin and flank determinants with novel regulatory inputs.

Aggression is an essential animal behavior for survival, particularly in situations where fighting cannot be avoided. In such situations, the choice of fighting strategy (eg biting, charging, or defending) is critical. Although the molecular bases of fighting and aggressiveness have been previously studied, how genetic, transcriptional, and neurobiological mechanisms contribute to the choice of fighting strategy remains largely unknown. Here, we use two subpopulations of chickens bred for cockfighting that show markedly different fighting strategies: offensive and defensive attack. A genome-wide screen comparing individuals from the two subpopulations indicated a polygenic background and we identified 15 candidate genes, five of which are implicated in neuronal development. Among these, the transcription factor gene FOXP1 was notable. FOXP1 is essential for neuronal development in the brain and has been implicated in the regulation of motor circuits. Transcriptomic analysis of the diencephalon also revealed differential expressions of genes involved in neurodevelopment, as well as in the synthesis and release of neurotransmitters. RNA-sequencing and immunohistochemistry suggested that activation of the indirect pathway of the brain motor circuit promotes the defensive fighting strategy. This was further supported by behavioral pharmacological experiments targeting dopaminergic signaling. Taken together, our results indicate that genomic variation and altered expression of neurodevelopment-related genes underlie differences in fighting strategies, and that the neuroendocrine changes in brain circuits further modulate these behavioral outcomes.

Eukarya resemble Archaea in DNA replication. Analysis of the DNA replication machinery of Asgard archaea may provide a valuable test of the hypothesis that this phylum is the origin of Eukarya. Among the replication proteins, primase, which comprises the catalytic subunit PriS and the non-catalytic subunit PriL, synthesizes primers for extension by DNA polymerase. Here, we show that Asgard primases fall into two major groups, denoted the Heimdall group and the Loki group, which are phylogenetically and structurally more closely related to eukaryotic primases and to primases from non-Asgard archaea, respectively. Notably, like human PriL, PriL of the Heimdall group possesses an extra C-terminal domain, which, absent in archaeal PriL of the non-Heimdall group, presumably serves to enhance the stability of the conserved iron-sulfur cluster in PriL. We overproduced and purified the PriS and PriL subunits of the Heimdall group from the Candidatus Gerdarchaeota archaeon B18_G1 in Escherichia coli. Biochemical characterization reveals that the B18_G1 primase is capable of primer synthesis and extension, preferentially using dNTPs as substrates, as shown for primases from non-Asgard archaea; however, unlike non-Asgard archaeal primases, it produces short primers, a feature typical of eukaryotic primases. These results shed significant light on the evolutionary pathway of primase and are consistent with the hypothesis of the Asgard origin of Eukarya.

Heterostyly is a floral polymorphism controlled by an S-locus supergene in several angiosperm families. Most heterostylous species are self-incompatible. Here, we investigate the genomic architecture of distyly in self-compatible Cordia subcordata in which incompatibility has apparently been lost. We assembled chromosome-level genomes of floral morphs and conducted population genomic analyses to locate the S-locus region. We used transcriptomic analyses of floral organs and functional validation by gene overexpression to identify genes controlling floral dimorphism. The tempo and mode of origin of S-locus genes was also investigated to determine whether gene duplication facilitated supergene assembly. The candidate S-locus in C. subcordata contained 12 genes, eight of which were restricted to the S-morph. CsGA2ox6 deactivates gibberellins and was exclusively expressed in S-morph pistils. Overexpression of CsGA2ox6 in transgenic tobacco produced flowers with shortened styles and an apparently functioning self-incompatibility system. The genomic locations of paralogs and estimations of duplication age suggested that the S-locus genes may have arisen through stepwise duplications, although an origin via segmental duplication could not be excluded. Our study revealed molecular convergence with several other distylous families in hemizygous structure and possibly in the mode of supergene origins. We also identified a molecular pathway for style-length control, likely through gibberellin deactivation by CsGA2ox6, which may have also controlled the expression of self-incompatibility in transgenic plants.

Venom has independently evolved across many lineages, yet relatively few have been studied in detail, particularly among insects. Of these, Neuroptera (lacewings, antlions, and relatives) remain largely unexplored, despite being widespread with agriculturally important groups such as green lacewings. While adults are nonvenomous, neuropteran larvae are ferocious predators that use pincer-like mouthparts to inject paralyzing and liquefying venom to subdue and consume their prey. Here, we provide a comprehensive investigation of the venom system in Neuroptera by integrating a high-quality genome, long-read transcriptomes spanning all life stages, microCT-reconstruction of venom glands, tissue-specific expression analyses, venom proteomics, and functional assays of the common green lacewing Chrysoperla carnea. We provide a re-description of the neuropteran venom system, demonstrate the venom's insecticidal and cytotoxic activity, and show that the venom comprises diverse toxin gene families and is richer and more similar to the venom of antlions than previously proposed. We show that this toxin arsenal is the result of a multitude of evolutionary events that include co-option, recruitment following gene duplication, diversification of toxin-paralogs by gene duplication, and functional innovation of new paralogs through both small structural and large architectural changes. In addition, we find that alternative splicing of toxin genes is an important contributor to the biochemical arsenal, which is a mechanism rarely documented among venomous animals. Our results demonstrate how multiple genomic and evolutionary mechanisms together contribute to the emergence and evolution of a complex molecular trait, and provide new insights into the evolution of venom in insects.

Paraspeckles are nuclear bodies essential for gene regulation and stress response, and they are built upon the long non-coding RNA NEAT1. Together with the syntenic MALAT1, these are the only lncRNAs that use the tRNA-processing machinery for maturation, yet they differ in function and evolutionary conservation. To investigate these differences, we identified NEAT1 and MALAT1 orthologs across 545 mammals. For NEAT1, we found that G-quadruplexes, short motifs interacting with DBHS proteins and TDP-43, long gene length, and self-complementary regions are highly conserved features that likely stabilize paraspeckle integrity. Transposable elements also contributed structural modules potentially recognized by DBHS proteins, underscoring their role in NEAT1 evolution. The NEAT1Short isoform was present in all orthologs, and the TDP-43-mediated isoform switch appears to be conserved. In contrast, MALAT1 function likely relies on its conserved primary sequence and regions under purifying selection. This is the first large-scale phylogenetic study of NEAT1 - a lncRNA that lacks sequence similarity between orthologs while maintaining functional and syntenic conservation.

Protein synthesis, while central to cellular function, is error-prone. The resulting mistranslation is generally costly, but we do not know how these costs compare or interact with the costs imposed by external selection pressures such as antibiotics. We also do not know whether and how these costs are compensated during evolution. It is important to answer these questions, since mistranslation is ubiquitous and antibiotic exposure is widespread. We quantified the growth cost of genetically increasing and decreasing mistranslation rates and exposure to low antibiotic concentrations in Escherichia coli. Mistranslation costs were generally lower than the cost imposed by antibiotics and exacerbated in a strain-specific manner under antibiotic exposure. All strains quickly compensated for the antibiotic cost during experimental evolution, via antibiotic- and genotype- specific mutations. In contrast, mistranslation costs were significantly reduced only in some cases, without clear causal mutations. Control populations that evolved without antibiotics consistently compensated for the cost of accuracy and evolved increased antibiotic resistance as a by-product. Our work demonstrates that even when the cost of mistranslation is weak, altered translation accuracy can shape adaptive outcomes and underlying genetic mechanisms, with strong collateral fitness effects for apparently unrelated phenotypes such as antibiotic resistance.

Gene duplication and transposable elements (TEs) are major drivers of genomic innovation that can fuel adaptation. While the roles of duplication and TE-driven diversification are documented in plant pathogens, they remain insufficiently explored in insect pests such as aphids, where olfactory (OR) and gustatory receptor (GR) genes are key to host recognition. We analyzed 521 OR and 399 GR genes, alongside TEs, across 12 aphid genomes with varying host ranges. Aphid lineages with broader host ranges exhibited higher evolutionary rates, driven by gene family expansions linked to host interaction, including lipid metabolism, immune function, and transposase activity. OR and GR genes evolved through proximal and tandem duplications and were shaped by diversifying selection, with bursts of positive selection followed by prolonged purifying selection, consistent with adaptation to novel hosts. Younger TEs were significantly enriched near OR genes compared to GRs and other genomic regions, suggesting a catalytic role of TEs in their diversification. However, OR proteins encoded by TE-associated ORs exhibited reduced functional potential. In contrast, GR proteins encoded by TE-associated GRs retained signatures of adaptation, as inferred from deep learning models predicting functionally important protein regions. These findings suggest that TE activity may facilitate functional innovation in GRs while alleviating constraints or pseudogenization in ORs. This study reveals how duplication, selection, and TE dynamics shape gene evolution in insect pests. It also provides the first chromosome-scale genome assembly of Dysaphis plantaginea, with comprehensive annotations and functional predictions of OR/GR genes, bridging adaptive evolution with mechanistic insights.