Biology subjects

Henschel, J.

Publications and source records attributed to Henschel, J..

3 recordsLinked to original sources

bioRxiv2026

Tracking a major evolutionary transition to superorganismality

Major transitions in evolution are associated with the loss of independent reproduction by formerly autonomous units. Termites provide a powerful system for studying this process because they exhibit diverse social systems in which worker developmental and reproductive potential declines with increasing colony-level organismality. However, the evolutionary sequence and developmental genetic basis of these transitions remain unresolved. Here, using comparative developmental transcriptomics across seven termite species that differ in workers' reproductive potential, we reconstructed the evolutionary history of termite social systems. We found that linear caste development, in which workers retain full reproductive potential, represents the ancestral state of termites. Bifurcated caste development, in which workers partially lose reproductive potential early in development, evolved independently multiple times, with two origins subsequently giving rise to superorganisms with unipotent, sterile workers. Ancestral gene regulatory network (GRN) reconstruction revealed that linear caste development evolved through retention of a juvenile-like worker state and co-option of a conserved developmental GRN characterizing hemimetabolous insect nymphal development, in which juvenile hormone, ecdysone and TGF-{beta} signaling pathways play central roles. The convergent evolution of bifurcated caste development repeatedly co-opted the GRN underlying linear caste development, heterochronically shifting its activity to earlier developmental stages. Finally, we found that the evolution of termite superorganisms involved somatization of the worker caste and co-option of a conserved endocrine GRN for terminal differentiation. Together, these findings uncovered repeated routes to reduced workers' reproductive potential through GRN co-option and highlight striking parallels between superorganism evolution in social insects and organismal evolution in metazoans.

evolutionary biology↗

bioRxiv2026

M-CSF drives alveolar macrophage plasticity during development and cytomegalovirus infection

Alveolar macrophages (AM), the most frequent resident immune cells of the lung, are at the first line of defence against respiratory pathogens and instruct structural lung cells, e.g. in tissue repair. They are long-lived and receive their terminal phenotypic imprint through signals originating from the unique location at the tissue-air interface, as well as through cytokines like granulocyte-macrophage colony-stimulating factor (GM-CSF) and transforming growth factor-{beta} (TGF-{beta}). However, the regulatory mechanisms governing their phenotypic plasticity, which is conceptually critical for their positioning and differentiation in early life and for their functional adaptation during infection, remain poorly defined. Here we explored respiratory tract infection with cytomegalovirus (CMV), which is closely linked to mammalian immune evolution. Complementary host-pathogen fate-mapping strategies revealed AM to constitute the bottleneck for efficient mouse (M)CMV infection. MCMV infection induced macrophage colony-stimulating factor (M-CSF) in the alveolar space, and culturing of AM in M-CSF led to a profound remodelling of morphology, immunophenotype, and transcriptional identity, e.g. it increased the expression of interferon-stimulated genes (ISG), which modulated susceptibility to infection. Notably, already at baseline recently differentiated neonatal AM across species retained an M-CSF-associated transcriptional program. This was linked to reduced permissiveness to respiratory MCMV infection in vivo. Overall, our findings identify the role of M-CSF-dependent signalling in conferring plasticity to AM, when it is most needed, particularly during early-life establishment and in response to viral infection.

immunology↗

bioRxiv2024

Dynamic role of monocytes and meningeal macrophages in bacterial meningoencephalitis

Macrophages in the meninges, especially in the dura mater sheathing the brain from the skull, are involved in the immune defense of the central nervous system (CNS). However, their site-specific origin and function, both in steady state and in bacterial CNS infections are incompletely understood. Using an intravenous model of streptococcal meningoencephalitis that mimics hematogenous dissemination in humans, we found that bacteria accumulated predominantly in the leptomeninges and dura, whereas invasion into the brain parenchyma was rare. However, monocyte infiltration into the leptomeninges and parenchyma strongly correlated with disease severity. In the dura, infection triggered activation and loss of resident macrophages, followed by rapid engraftment of inflammatory monocytes that transiently replenished the dural macrophage niche. Under homeostasis, dural monocytes were supplied independently of CCR2 from adjacent skull bone marrow. In infection, however, this local reservoir was rapidly exhausted, and the markedly increased demand for monocytes required mobilization from peripheral bone marrow sources, revealing context-dependent heterogeneity in monocyte origin. Infection also reshaped ontogeny of this differential monocyte output, with an increase in Monocyte-Dendritic Cell Progenitor - derived monocytes (MDP-Mo). MDP-Mo exhibited enhanced MHC-II expression and persisted in the brain during the resolution phase together with CD4 T cells, suggesting a role in antigen presentation after bacterial clearance. Together, these findings reveal a highly dynamic and compartment-specific remodeling of monocyte ontogeny, recruitment, and differentiation across CNS borders during bacterial meningoencephalitis. These mechanisms may offer opportunities for therapeutic interventions in the future. One Sentence SummaryStreptococcal meningoencephalitis disrupts homeostatic, skull bone marrow-derived monocyte and macrophage trajectories in the dura.

immunology↗