BioEssays最新文献

Recent discoveries of transposable element (TE) activity in the octopus genome suggest, to some, that these "jumping genes" facilitated the evolution of cephalopod brains and possibly contribute to cognitive flexibility in these animals. In contrast, TEs are often regarded as genomic parasites with net deleterious effects on host fitness. The octopus genome provides an opportunity to compare these proposals to a genome-ecological alternative. We review evidence of TE accumulation and somatic activity, showing compatibility with both organism-beneficial and selfish-DNA interpretations. To resolve this, we apply ecological thinking within the genome to generate novel predictions. If TEs are adapted to a "requirement niche" typically found in germline cells, then TE-population growth rates (replication rates) should be nonnegative under similar "environmental" conditions (e.g., similar gene expression patterns to testes). This invites a comparison of expression levels across tissues. It is reasonable to infer some organism-beneficial function only when TE expression levels deviate from those predicted by the degree of niche-overlap with germline cells.

Biological systems maintain homeostasis, ensuring stability in the face of internal and external perturbations and counteracting stochastic noise. Traditionally, this is understood through the lens of control mechanisms designed to offset variations and maintain certain quantities near functionally desired set points. Here, we propose an alternative perspective to understand homeostasis: the collective dynamics perspective, in which homeostasis emerges spontaneously from high-dimensional interactions, creating limiting manifolds in phase space. These multi-dimensional attractor manifolds can constrain many components collectively, eliminating the need for explicit control of individual variables. The presence of null directions on a manifold allows for degenerate states that can add flexibility while preserving functionality. Using single-cell growth and division homeostasis as a test case, we develop and support our perspective by models and meta-analysis of numerous single-cell datasets across organisms and conditions. Importantly, we do not reject the control-theory perspective but rather suggest that control circuit models can be seen as low-dimensional projections of a more complex, multi-dimensional system.

Visual systems appear like homogenous structures, where identical functional units repeat themselves across the eye. This architecture is thought to ensure a uniform sampling of the surrounding environment. Furthermore, anatomically and functionally identical properties of single units belonging to the same cell type, yet located across retinotopical positions are thought to ensure translational invariance. At the same time, regional differences and stochastic variations in microcircuit architecture have been linked to the processing of specific visual features. Recent access to connectomic datasets has revealed heterogeneity in visual circuitry that is at odds with these criteria: Cells considered to belong to the same type are variable in number and identity of connected partners, as well as in the relative number of synapses. This variable connectivity suggests that heterogeneous computations, even within defined cell types, is the rule, rather than the exception. It is therefore an exciting question whether these network properties increase functional variability, or even functional robustness, of visual processing.

Recent advances in live-cell imaging, super-resolution microscopy, labeling techniques and cryo-electron microscopy reveal vimentin intermediate filaments (VIFs) as adaptable polymers that couple mechanical stability with rapid remodeling. In this review, we highlight recent findings and discuss how VIFs function as dynamic, interpenetrating networks with actin microfilaments and microtubules, coordinating cytoskeletal architecture while simultaneously facilitating organelle positioning and influencing cellular behavior. We also propose a hybrid transport model to capture the diverse modes of VIF cellular interactions. This emerging framework positions VIFs as dynamic integrators of cytoskeletal organization and intracellular logistics, with broad implications for understanding cell mechanics, migration, and disease.

Autoimmune diseases such as multiple sclerosis (MS) and rheumatoid arthritis (RA) involve complex interactions between local tissues and the immune system. Here, we highlight the immunological parallels between the central nervous system (CNS) meninges and the synovial joint, two sites traditionally considered immune-privileged. Both harbor resident immune cells and lymphatic vessels and support the formation of tertiary lymphoid organs (TLO) during chronic inflammation. In MS, meningeal TLO contributes to cortical grey matter damage, while in RA, synovial TLO drives joint destruction. T peripheral helper (Tph) cells, a subset of CD4⁺ T cells, are key players in both conditions by supporting B cell activation and autoantibody production. Epstein–Barr virus (EBV) infection, particularly in B cells within TLO, is implicated in the pathogenesis of both diseases. Targeting EBV-infected B cells, depleting Tph cells, or disrupting TLO represent promising therapeutic strategies for controlling disease progression and severity in MS and RA.

Recently, Nature published a large-scale analysis (“Dated gene duplications elucidate the evolutionary assembly of eukaryotes” by Christopher Kay and co-workers) that seems to put an end to symbiogenic models for eukaryogenesis. They state that the pre-mitochondrion arrives late, after practically all of the signature eukaryotic characteristics have evolved independently. However, this conclusion is based on reconstructed timescales for the gene duplications allowing these crucial eukaryotic cell functions. The reconstruction might be fundamentally flawed, because enhanced internal ROS formation upon endosymbiont entry would lead to both high mutation rates and strong selection for antioxidant as well as repair functions. As the endosymbiont had co-evolved with molecular oxygen, while the archaeal host had not, a phylogenetic analysis might misconstrue the higher rate of change in the host as indicative of much longer timescales for host gene duplications.

In article 70110, Bhattacharya et al. discuss the causes of coral bleaching, which results in a ghostly white appearance of colonies due to photosymbiont loss. Algal expulsion is widely considered an act of defense by corals to survive oxidative stress produced by these cells under heat (or other) stress. Using recently generated multi-omics and genetics data, the authors surmise that coral bleaching is in fact a multifactorial response that reflects a wide array of causes and effects and is often population specific. This perspective suggests that a “personal genomics” approach to coral conservation may prove useful to protect endangered reefs.

A novel model recently proposed by Doktorova et al. challenges current concepts for the molecular organization of the plasma membrane bilayer. It is at odds with previously published research. The model posits that there are far fewer phospholipid molecules in the outer leaflet of the bilayer than in the inner leaflet and that the resulting area deficit is filled by cholesterol. This conclusion is based on the incomplete hydrolysis of the phosphatidylcholine in intact erythrocytes by phospholipase A2, leading to the inference that the undigested fraction is endofacial. But the incomplete digestion can be explained by product inhibition. Furthermore, ultrastructural analysis has shown that almost all of the phosphatidylcholine in the erythrocyte bilayer resides in the outer leaflet. Finally, the high concentration of cholesterol predicted for the outer leaflet of resting human erythrocytes is not detectable by probes. The conflict of the new model with the literature makes it insecure.

The mastery of fire transformed human evolution through advantages spanning diet, behavior, physiology, and ecology. While these benefits are well established, here we highlight a previously overlooked cost — and selective pressure — unique to humans: high-temperature burn injury. Unlike other species, humans and their hominin ancestors have faced increased lifetime risk of burns, which we argue has driven genetic adaptation. Drawing on comparative genomic evidence across primates, we suggest that genes associated with burn injury response — relating to wound healing and inflammation — show signs of accelerated evolution in humans. We propose that recurrent exposure to burns acted as a selective force in our lineage, helping to explain both beneficial adaptations and paradoxical maladaptive responses to severe injury. By framing burns as an evolutionary pressure, the Burn Selection Hypothesis invites a re-evaluation of how fire shaped human biology and offers new perspectives for understanding both the evolutionary past and modern burn care.