Colony morphogenesis regulates sporulation dynamics in bacterial biofilms
In multicellular systems, organized phenotypic heterogeneity emerges from the interplay of processes spanning scales from molecular to population-level. Using Bacillus subtilis, we investigated feedback between the collective process of colony expansion and the distribution of spore development among individual cells, a process triggered by starvation. Biofilms are commonly studied using a strain with inhibited sporulation. Intact regulation yielded high-frequency sporulation early in biofilm growth. Biofilm composition was organized by a wave of sporulation driving biofilms toward dormancy from within. However, expansion was also maintained by non-sporulating cells in a narrow front at the external edge. Along with mathematical modeling, we also used mutants with altered biofilm morphogenesis to probe the relationship between colony expansion and sporulation. Sporulation dynamics were patterned by radial expansion, but the faster biofilms spread, the greater the separation of growth and sporulation distributions. We demonstrate essential interplay between cell behavior and the physics of collective expansion that organizes differentiation among cells.
### Competing Interest Statement
The authors have declared no competing interest.
National Institute of General Medical Sciences, R35GM142584, R35GM156451
U.S. National Science Foundation, PHY-2118561
Burroughs Wellcome Fund
📰 "A dual-phase enhancer couples progenitor maintenance and pancreatic lineage stability"
https://www.biorxiv.org/content/10.64898/2026.02.11.705016v1?rss=1 #Morphogenesis #CellA dual-phase enhancer couples progenitor maintenance and pancreatic lineage stability
Enhancers orchestrate transcriptional programs that control organ development and maintain differentiated cell states, yet how individual enhancers integrate developmental and long-term tissue maintenance logic remains poorly understood. Here, we identify a distal enhancer downstream of ptf1a (z3'-DpE) as a regulatory node coupling pancreatic development with acinar cell homeostasis in zebrafish. Deletion of z3'-DpE reduces ptf1a expression in pancreatic multipotent progenitor cells (MPCs), leading to depletion of the progenitor pool, altered morphogenesis, and premature exocrine differentiation. Transcriptomic analysis reveals broad repression of proliferation- and morphogenesis-related genes, including Notch pathway components essential for progenitor maintenance. After differentiation, loss of z3'-DpE contributes to acinar cell loss, expansion of ductal and endocrine compartments, and disrupted pancreatic architecture. Chromatin-accessibility profiling of purified acinar cells reveals that reduced ptf1a activity leads to widespread remodeling of the acinar chromatin landscape, with decreased accessibility at loci associated with acinar identity and developmental programs, and increased accessibility at sites linked to inflammation, epithelial plasticity, and pancreatic cancer susceptibility. Histopathological analysis shows disorganized acinar tissue with increased duct-like structures and mucinous lesions reminiscent of early pancreatic neoplasia. Thus, z3'-DpE safeguards acinar identity by sustaining ptf1a expression and a chromatin landscape that restricts fate instability and pathological plasticity. Our findings demonstrate the mechanistic sufficiency of a single enhancer to coordinate progenitor expansion and long-term lineage stabilization, providing a paradigm for how a developmental regulatory element is redeployed to preserve tissue integrity and suppress disease-associated plasticity.
### Competing Interest Statement
The authors have declared no competing interest.
Tissue phase transitions in development: more than just mechanics
Summary: Tissue material phase transitions are classically thought to regulate tissue deformability. This Review emphasises their unexpected roles in directly influencing growth and patterning signalling dynamics during development.
📰 "A dialog between cell adhesion and topology at the core of morphogenesis"
https://arxiv.org/abs/2602.09867 #Cond-Mat.Stat-Mech
#Cond-Mat.Soft
#Morphogenesis #Q-Bio.To
#Cell
A dialog between cell adhesion and topology at the core of morphogenesis
During the development of an organism, cells must coordinate and organize to generate the correct shape, structure, and spatial patterns of tissues and organs, a process known as morphogenesis. The morphogenesis of embryonic tissues is supported by multiple processes that induce the precise physical deformations required for tissues to ultimately form organs with complex geometries. Among the most active players shaping the morphogenetic path are fine-tuned changes in cell adhesion. In this paper, we show that a local, pair-wise property defined at the cell-cell contact level has important global consequences for embryonic tissue topology, being determinant in defining both the geometric and material properties of early embryo tissues.
Force-dependent stabilization of apical actomyosin by Lmo7 during vertebrate neurulation
Coordinated control of actomyosin contractility is essential for epithelial morphogenesis, including vertebrate neural tube closure. Lim domain only 7 (Lmo7) is a force-sensitive regulator of contractility that binds non-muscle myosin II (NMII) heavy chain to initiate apical constriction (AC) during Xenopus neural tube closure. Lmo7 is not required for actomyosin pulsatile activity or changes in the junction length in the intercalating cells during anteroposterior axis elongation. However, Lmo7 knockdown fails to stabilize actomyosin at the apical cortex at the onset of neural tube folding. Gain-of-function approach in gastrula ectoderm confirms a role for Lmo7 in actomyosin stabilization. Mechanistically, force-dependent dephosphorylation of Ser355 in the Lmo7 myosin binding domain enhances Lmo7 binding to NMII and increases NMII abundance at the apical cortex. Notably, initially homogeneous expression of Lmo7 in ectoderm cells progressively leads to apical domain heterogeneity that tightly correlates with Lmo7 levels, arguing for a positive feedback regulation between mechanical forces and Lmo7 activity. We propose that the force-dependent binding of Lmo7 to NMII stabilizes both proteins at the apical cortex, triggering enhanced apical constriction.
### Competing Interest Statement
The authors have declared no competing interest.
NIH Common Fund, R35GM122492
📰 "Amorphous-to-Rodlet Structural Transition Governs the Interfacial Functions of Aspergillus oryzae Hydrophobin RolA"
https://www.biorxiv.org/content/10.64898/2026.02.08.702184v1?rss=1 #Morphogenesis #CellAmorphous-to-Rodlet Structural Transition Governs the Interfacial Functions of Aspergillus oryzae Hydrophobin RolA
Hydrophobins are low–molecular–weight biosurfactant proteins that coat the cell surface of filamentous fungi, making it hydrophobic and supporting morphogenesis. On conidia, hydrophobins self–assemble to form rod–shaped multimeric structures known as rodlets. Previously, we reported that hydrophobin RolA from the industrial fungus Aspergillus oryzae first forms an amorphous film at the air–water interface and then undergoes structural rearrangement to form a densely packed rodlet film. This raised the question of whether the amorphous or the rodlet film is more important for the biological functions of RolA. In this study, to compare the properties of amorphous films with those of rodlet films, we used RolA mutants that had lost the ability to form rodlets and therefore remained in the amorphous state. We found that the rodlet film was more rigid than the amorphous film and had stronger surface activity and a greater capacity to change surface wettability. RolA altered the properties of A. oryzae conidia only when it was in the rodlet state. These findings highlight the functional versatility of RolA and show that their dynamic structural transitions directly modulate their function.
### Competing Interest Statement
The authors have declared no competing interest.
Japan Society for the Promotion of Science, Grant-in-Aid for Scientific Research (B), Grant-in-Aid for JSPS Fellows
Noda Institute for Scientific Research
📰 "Adenocarcinoma cell mechanobiology is altered by the loss modulus of the surrounding extracellular matrix"
https://www.biorxiv.org/content/10.64898/2026.02.04.703912v1?rss=1 #Morphogenesis #Extracellular #Cell📰 "Analysis of the assembly, stabilization and maturation of the multiphasic TAZ biomolecular condensates"
https://www.biorxiv.org/content/10.64898/2026.01.29.702607v1?rss=1 #Morphogenesis #Cell
Rxiv mechanobio