The research team collected scale-leaf tissue from M. callistoma in Shiyan, Hubei Province, and sequenced it on an Illumina HiSeq 4000 platform at a mean depth of over 900-fold. Assembly with GetOrganelle and polishing with Pilon produced a single circular plastome of 29,784 base pairs with a GC content of 30.8 percent. That figure might sound unremarkable until compared with a typical photosynthetic plant, whose plastome runs roughly 150,000 base pairs and carries more than a hundred genes. The M. callistoma plastome contains just 40 genes: 20 protein-coding genes, 16 transfer RNAs, and four ribosomal RNAs. Strikingly, the canonical quadripartite structure found in almost all land plant plastids, with two inverted repeats separating large and small single-copy regions, is entirely absent. No inverted-repeat boundaries could be detected at all.

The gene inventory tells the story of a genome in terminal decline. Every photosynthetic function has been erased. There are no photosystem subunits, no NADH dehydrogenase genes, no cytochrome b6f complex components, no ATP synthase subunits, and no rubisco large subunit. What remains is essentially a minimal housekeeping kit: ten genes for small ribosomal subunit proteins, seven for large subunit proteins, and just three other coding genes, infA, matK, and accD. Four of the retained genes carry a single intron. This is the genomic signature of an organelle whose core reason for existence, photosynthesis, has been outsourced to fungal partners, leaving relaxed selection to strip away everything the plant no longer needs.

To place this genome in context, the researchers compiled published plastomes from 30 mycoheterotrophic species across six families, ranging from orchids such as Gastrodia and Lecanorchis to the bizarre holoparasites Sciaphila and Mitrastemon. The comparison revealed a spectrum of decay. Sciaphila thaidanica and Mitrastemon yamamotoi carry plastomes of only about 20 kilobases, among the smallest known in flowering plants, while at the other extreme some Burmannia species retain genomes approaching 100 kilobases. GC content showed a weak but statistically significant positive correlation with genome size, suggesting that as these genomes shrink, their nucleotide composition shifts in parallel. Within Monotropoideae itself, Pterospora andromedea holds the largest plastome at roughly 40 kilobases, while the more recently diverged Monotropa uniflora has the smallest at about 27 kilobases.

Whole-genome alignments exposed another dimension of decay: the collapse of synteny, the conserved order of genes along the chromosome. Among Monotropoideae species, gene order is scrambled, particularly in Hypopitys, Monotropsis, Monotropastrum, and Monotropa. Fragment loss has accumulated in more recently diverged lineages, so that even within the genus Monotropa, where synteny is relatively well preserved, the overall picture across the subfamily is one of progressive disintegration. Ancestral-state reconstruction across the 30 species showed that losses of the large genes ycf1 and ycf2 occurred convergently among eudicot lineages, while all sampled Monotropa species lacked rps23, pointing to a lineage-specific loss within that genus.

The phylogenomic analysis went beyond genome description to resolve long-standing questions about relationships within Ericaceae. Using a concatenated alignment of plastid protein-coding genes nearly 48,000 base pairs long, with Actinidia chinensis as an outgroup, the team recovered a well-supported split into two major clades. Clade 1 united Pyroloideae, Arbutoideae, and Monotropoideae, with Pyroloideae branching earliest and Monotropoideae emerging as the youngest lineage. Within Monotropoideae, the sampling covered 10 of the 12 recognized genera and achieved maximum bootstrap support of 100 for the backbone. Pterospora and Sarcodes occupied successive early-branching positions, followed by Pleuricospora, while a clade of Monotropsis, Monotropastrum, and Monotropa was sister to a group containing Allotropa, Hemitomes, Pityopus, and Hypopitys. Clade 2 comprised the core Ericaceae, subdivided into Vaccinioideae and Ericoideae.

Divergence dating with fossil calibrations placed the split between Pyroloideae and the remaining subfamilies at approximately 67.77 million years ago, in the latest Cretaceous. Arbutoideae and Monotropoideae diverged around 66.57 million years ago, and diversification within Monotropoideae began about 63.35 million years ago, immediately after the end-Cretaceous extinction. The genus-level splits came much later: Sarcodes and Pterospora separated roughly 45.79 million years ago, Monotropsis split from the lineage leading to Monotropa and Monotropastrum about 39.73 million years ago, and those two genera diverged about 26.74 million years ago. The rapid radiation of Rhododendron and Vaccinium, by contrast, occurred only around 1 to 2 million years ago.

Perhaps the most striking finding concerns geography. Ancestral-range estimation using the DIVALIKE+J model in RASP placed the most recent common ancestor of Clade 1 in Asia during the late Cretaceous to early Cenozoic. From there, the lineage dispersed to North America, most plausibly across the Bering Land Bridge, which connected the continents from the latest Cretaceous into the early Paleocene, when a warm, humid belt of deciduous broadleaf forest stretched across the region. Then came a remarkable reversal: the ancestor of the Monotropsis, Monotropastrum, and Monotropa lineage appears to have dispersed back to Asia during the late Eocene to early Oligocene, around 39.70 million years ago, giving rise to the East Asian endemics Monotropastrum humile and Monotropa callistoma. The ghost plants, in other words, crossed the world twice.

The comparative analysis also yielded a testable hypothesis about the order in which plastid genes are lost as plants abandon photosynthesis. Across the 30 species examined, the ndh genes were absent everywhere, followed by photosystem, cytochrome, rubisco, and ycf3/4 genes, then the RNA polymerase genes, then atp genes, and finally the ribosomal, transfer RNA, and housekeeping genes such as accD, clpP, and matK. The sole exception was Burmannia cryptopetala, which retains atp genes, a pattern associated with mixotrophic or partially parasitic lifestyles. The team proposes that the degree of a plant’s absolute dependence on fungal hosts correlates with the breadth of plastid gene loss, with Monotropa, whose plastid genes evolve roughly 13 times faster than its nuclear genes, representing an advanced stage of degradation in which even clpP has been discarded.

Yet the decay is not random, and that is the deeper lesson of the study. Housekeeping genes persist with remarkable consistency: accD, which catalyzes the first committed step of fatty acid biosynthesis and is essential for building the plastid’s own membranes, was retained in every single mycoheterotrophic species examined. The retention of matK across all Monotropoideae and Burmanniaceae, despite its patchy record in orchids, and the lineage-specific survival of ycf1 and ycf2 in some orchids and Burmanniaceae but not others, show that different lineages face different residual functional constraints. The endpoints of plastid genome reduction form a spectrum rather than a single destination, ranging from the streamlined but intact genomes of Monotropoideae to the complete loss of the plastid genome in Balanophora, which has transferred even accD to the nucleus. When an organelle’s core function is outsourced, its genetic system converges, again and again across independent lineages, toward the same extreme simplification. The ghost plants of Asia and North America, silent and white beneath the forest canopy, are carrying out that experiment in real time, and their genomes are the record.

Subject of Research: Plastome evolution and phylogenomics of the mycoheterotrophic subfamily Monotropoideae (Ericaceae)

Article Title: Phylogenomics Clarifies Plastome Reduction and Phylogenetic Relationships in Monotropoideae

Article References: Deng, G., Duan, K., Xiang, N., Gao, F., Zhan, P., Shu, R., Lin, Q., Zuo, Q., & Yuan, T. (2026). Phylogenomics Clarifies Plastome Reduction and Phylogenetic Relationships in Monotropoideae. Ecology and Evolution, 16(10), Article e74449. https://doi.org/10.1002/ece3.74449

Image Credits: AI Generated

DOI: 10.1002/ece3.74449

Keywords: Monotropoideae, mycoheterotrophy, plastome reduction, Ericaceae, Monotropa callistoma, phylogenomics, Bering Land Bridge, biogeography, gene loss, relaxed selection, ghost plants, divergence dating

The research team, led by Vinita Lamba, Andrew J. Alverson, and Xuan Zhuang of the University of Arkansas, together with Jacob M. Daane of the University of Houston, set out to systematically identify gene-inactivating mutations across the cryonotothenioid radiation, the lineage of notothenioid fishes that diversified after the Southern Ocean cooled to its present near-constant low temperatures. What makes this group especially powerful for such an analysis is the availability of non-Antarctic notothenioid outgroups. Because these relatives live in warmer waters and retain many ancestral genes, researchers can infer which genes were present in the common ancestor and therefore pinpoint which losses occurred specifically after the Antarctic lineage became established.

Methodologically, the study is notable for its rigor. The researchers used whole-genome alignments and orthology-aware comparative analyses spanning eleven cryonotothenioid species and four non-Antarctic outgroups. Orthology-aware analysis means the team carefully tracked which genes correspond to which across species, distinguishing true gene loss from mere annotation gaps or assembly errors. To reduce reference bias, a common pitfall in comparative genomics where results are skewed by the choice of reference genome, the authors applied stringent filters. They also excluded any candidate lost loci that showed detectable transcriptomic support, meaning that if a gene appeared to be missing from the genome but was still being transcribed, it was removed from consideration. This conservative approach was designed to ensure that the final catalog reflects genuine losses of coding potential rather than artifacts of sequencing, assembly, or annotation.

After these filters, the team identified 30 high-confidence single-copy orthologs with loss of coding potential across the sampled cryonotothenioids but intact coding sequences in the outgroups. Single-copy orthologs are particularly informative because they exist as one copy per genome in the ancestor, so their loss cannot be masked by a duplicate gene stepping in to perform the same function. The fact that these losses are shared across the Antarctic clade suggests they occurred near the base of the radiation, early in the group’s polar history, and have since become part of the inherited genomic background on which all subsequent specialization was built.

The functional categories of the lost genes are striking. They include genes associated with lipid and amino acid metabolism, water transport, renal glucose reabsorption, skeletal mineralization, circadian regulation, and tRNA modification pathways. Each category hints at physiological adjustments that may have accompanied life in the Southern Ocean. Lipid metabolism genes, for example, could relate to the demands of maintaining membrane fluidity and energy storage in the cold. Water transport and renal glucose reabsorption genes may reflect the osmoregulatory challenges of a stable, cold marine environment. Circadian regulation losses are especially intriguing given the extreme seasonal light cycles of polar regions, where the sun disappears for months at a time, potentially relaxing the selective pressure on molecular clocks tuned to daily rhythms.

Beyond the clade-wide losses, the study identified 12 additional single-copy orthologs that have been lost across the examined icefishes, the famous white-blooded family of Antarctic fish, while being retained in red-blooded notothenioids and in the outgroups. The icefish family, Channichthyidae, is already celebrated for its extraordinary loss of hemoglobin expression, making it the only vertebrate group whose adults lack functional red blood cells. The new findings extend this pattern of loss into other genes associated with oxygen transport, iron handling, erythroid biology, and vesicular trafficking. Erythroid biology encompasses the development and maintenance of red blood cells, so additional losses in this pathway are consistent with the icefishes’ radical evolutionary departure from oxygen-carrying blood. Vesicular trafficking genes, meanwhile, point to changes in how cells move materials internally, a process that intersects with iron metabolism and membrane biology in ways that may be linked to the icefishes’ unusual blood physiology.

One of the most compelling aspects of the catalog is that many of the lost genes are conserved across vertebrates and are associated with disease-relevant phenotypes in humans or model organisms. In laboratory genetics, a knockout is a deliberately engineered disruption of a gene used to study its function, and knockout organisms often display developmental defects, metabolic disorders, or other pathologies. The Antarctic fishes, by contrast, carry these loss-of-function variants in viable, reproducing wild populations that thrive in one of Earth’s most demanding environments. This makes them a natural comparative system for studying how loss-of-function mutations can persist and even become fixed in a lineage without causing overt harm.

The authors frame these candidate natural knockouts as a source of testable hypotheses about the mechanisms that allow vertebrates to tolerate gene loss. Three broad mechanisms are proposed. Environmental buffering refers to the possibility that the stable, cold Southern Ocean environment reduces the selective cost of losing certain functions; if a gene’s role becomes unnecessary under constant conditions, its loss may be effectively neutral. Paralog compensation occurs when another member of the same gene family takes over the lost gene’s function, cushioning the impact of the knockout. Pathway rewiring describes deeper evolutionary restructuring, in which metabolic or regulatory networks are reorganized so that the lost gene’s contribution is no longer needed. Disentangling which mechanism applies to which locus is now an open empirical question, and the catalog provides the raw material for such investigations.

The study also underscores a broader point about genome evolution: gene loss is a major but often underappreciated mode of evolutionary change. Genomes are frequently discussed in terms of what they gain, through duplication and innovation, but what they lose can be equally consequential. Once a loss event becomes fixed in a population, it permanently alters the inherited gene complement and can constrain or redirect the evolutionary trajectories available to descendant lineages. Shared losses near the base of a radiation, as seen here, effectively set the stage for later specialization, meaning that the icefishes’ dramatic adaptations were built atop a genomic foundation already shaped by earlier deletions and inactivations.

Funded in part by the U.S. National Science Foundation, including a CAREER Award to Xuan Zhuang, the work opens a window onto vertebrate physiology under chronic cold that no laboratory model could easily replicate. As genome assemblies for polar species continue to improve, the natural knockout catalog of the notothenioids is likely to grow, and each entry represents an invitation to ask a deceptively simple question: what happens when a vertebrate loses a gene that humans and model animals cannot live without? For the fishes of the Southern Ocean, the answer has been unfolding for millions of years, written in the absences scattered across their genomes.

Subject of Research: Comparative genomics of gene loss in Antarctic notothenioid fishes

Article Title: Gene loss under constant cold reveals “natural knockout” loci in Antarctic notothenioid fishes

Article References: Lamba, V., Alverson, A. J., Daane, J. M., & Zhuang, X. (2026). Gene loss under constant cold reveals “natural knockout” loci in Antarctic notothenioid fishes. BMC Genomics. https://doi.org/10.1186/s12864-026-13346-x

Image Credits: AI Generated

DOI: 10.1186/s12864-026-13346-x

Keywords: gene loss, Antarctic notothenioids, icefish, comparative genomics, natural knockout, genome evolution, molecular evolution, Southern Ocean, hemoglobin, evolutionary physiology, orthology, cold adaptation

Salmonella Typhimurium is among the leading causes of foodborne gastroenteritis worldwide, and its monophasic variant—distinguished serologically by the absence of one of its two flagellar phases—has surged in prevalence across Europe, the Americas and Asia over recent decades. The lineage, which belongs to sequence type 34 and typically displays the antigenic formula 4,[5],12:i:-, has repeatedly been implicated in outbreaks linked to pork, poultry and processed foods. Yet despite its clear epidemiological importance, the genetic determinants that allowed this clone to outcompete its biphasic ancestor, the previously prevalent ST19 lineage, had remained uncertain. The new study set out to resolve that question at unprecedented scale.

The team’s comparative analysis of tens of thousands of genomes revealed a striking pattern: the expanding ST34 clone carried a frameshift mutation in dinB, the gene encoding a translesion DNA synthesis polymerase also known as DNA polymerase IV. The mutation, a deletion of a single thymine residue within a homopolymeric tract of seven thymidines near the 5′ end of the gene, introduces a premature stop codon that truncates the 39.7-kilodalton DinB protein to a nonfunctional fragment of roughly 1.9 kilodaltons. Because DinB is normally involved in bypassing damaged DNA templates and in generating genetic diversity under stress, its loss initially appears counterintuitive for a pathogen on the rise.

Functional experiments, however, demonstrated that the crippled polymerase has far-reaching downstream consequences. Transcriptomic profiling showed that the frameshift dinB mutation rewires the expression of flagellar genes, altering the balance between the two phase-one and phase-two flagellin systems that Salmonella uses to evade host immune detection. Specifically, the mutation led to transcriptional changes that favored retention of fliC, which encodes phase-one flagellin, and set the stage for the subsequent loss of fljB, the gene encoding phase-two flagellin. Western blot analyses confirmed that dinB-mutant strains displayed an increased proportion of cells expressing FliC, while in vitro motility assays showed that swimming ability was preserved despite the underlying genetic upheaval.

The physiological consequence of this reprogramming became apparent in infection models. Using transposon insertion sequencing and in vivo competition experiments in mice, the researchers found that the requirements for successful gut colonization shifted once fljB was lost. Genes that were dispensable, or even costly, in the ancestral background became essential or advantageous in the mutant context, and vice versa. The frameshift dinB strain carrying the fljB deletion outcompeted the previously prevalent biphasic ST19 lineage in the intestine, indicating that the combination of the polymerase defect and flagellin loss conferred a measurable competitive advantage within the host environment.

To move beyond correlation, the authors built a temporal evolutionary model that simulated the dynamics of four competing lineages: biphasic ST19, biphasic ST34, ST34 carrying the frameshift dinB, and monophasic ST34 carrying both the frameshift and the fljB deletion. The modeling demonstrated that the chronological order of the events matters critically. The dinB mutation had to precede the loss of fljB for the monophasic clone to expand as observed, and the simulated selection coefficients derived from the model were quantitatively consistent with selection estimates computed from real-world changes in genotype frequencies among human clinical isolates. Sensitivity analyses confirmed that the conclusion held regardless of the initial frequency of ST34, the presence or absence of spatial population structure, or the precise metric used to quantify selection.

This ordered dependency is what the researchers describe as a stepwise pathoadaptation model: a sequence of gene-loss events in which each deletion reshapes the genetic background so that the next loss becomes beneficial rather than deleterious. The concept echoes a growing recognition in microbial evolution that genome reduction can be a creative force. Recent work on Vibrio parahaemolyticus, for example, showed that wave succession within a pandemic clone was likewise driven by gene loss, and earlier studies documented how monophasic Salmonella Typhimurium microevolved during a prolonged epidemic in the United Kingdom. The new study, however, is notable for linking the ecological success of a zoonotic lineage to a specific, mechanistically validated chain of molecular events.

The broader implications extend to public health forecasting. If the emergence of major bacterial clones can depend on relatively simple, ordered mutational steps, then surveillance systems that monitor homopolymeric tracts and other mutation-prone loci may gain predictive power over which lineages are poised to expand. The study’s data resources—including genomic data deposited at the China National GeneBank Database, Enterobase and NCBI, transcriptomic data under accession GSE280131, proteomic data via PRIDE, and transposon-sequencing reads under BioProject PRJNA1347559—provide a substantial foundation for such efforts. The mathematical model code has also been made publicly available on GitHub, enabling other groups to test the generality of the sequential gene-loss framework in other pathogens.

At the same time, the work underscores how little of bacterial adaptation is driven by gene acquisition alone. Monophasic ST34 also carries traits such as copper resistance and heavy-metal tolerance that have been implicated in its persistence in livestock production environments, and antimicrobial resistance remains a defining feature of many circulating clones. But the new analysis places gene loss at the center of the lineage’s rise, reframing flagellar phase variation—a long-studied quirk of Salmonella biology—as a decisive axis of clonal competition. As the authors note, understanding the genetic factors facilitating the emergence of infectious diseases is critical, and this study delivers a concrete mechanistic answer for one of the most consequential zoonotic pathogens of the modern food system. The lesson is uncomfortable but clarifying: for bacteria, sometimes less is more, and the road to pandemic status can be paved by the genes a pathogen leaves behind.

Subject of Research: Stepwise gene loss driving the clonal expansion of monophasic Salmonella Typhimurium ST34

Article Title: Sequential gene loss promotes expansion of monophasic Salmonella Typhimurium ST34

Article References: Wu, X., Wang, T., Jia, C., Zhou, H., Li, Y., Baker, S., & Yue, M. (2026). Sequential gene loss promotes expansion of monophasic Salmonella Typhimurium ST34. Nature Microbiology. https://doi.org/10.1038/s41564-026-02483-4

Image Credits: AI Generated

DOI: 10.1038/s41564-026-02483-4

Keywords: Salmonella Typhimurium, monophasic ST34, gene loss, dinB, flagellin, fljB, pathoadaptation, bacterial evolution, genomic epidemiology, foodborne pathogen, zoonotic disease, Nature Microbiology