Search bioRxiv⌕ Search

bioRxiv · 10.64898/2026.05.24.727559

A Data-Driven Correction Framework for Axial- and Radial-Position-Dependent Intensity Attenuation in Volumetric Fluorescence Microscopy

Abstract

Accurate quantification of fluorescence signals in three-dimensional (3D) microscopy is often hindered by axial- and radial-position-dependent attenuation, limiting reliable measurements in live biological specimens. Here, we present a data-driven statistical correction model that compensates for signal loss arising from axial- and radial-position in 3D time-lapse imaging of Caenorhabditis elegans embryos. Our framework incorporates axial position (imaging depth, z), radial position (distance from the center of the field of view, r), together with cell cycle progression, to recover cell-specific fluorescence intensities independent of axial- and radial-positions. By leveraging repeated observations of biologically comparable states, the model infers attenuation directly from the data without requiring external calibration. Notably, the sign of the inferred radial-position-dependence in biological specimens was opposite to that observed in homogeneous fluorescent reference samples, underscoring the value of specimen-specific, data-driven correction. Validation using histone-tagged fluorescent proteins demonstrated that the method effectively removes geometric bias in nuclear fluorescence signals, enabling consistent quantification across cells and embryos. This approach provides a robust and generalizable solution for correcting intensity attenuation in volumetric microscopy datasets, thereby enabling more accurate and reproducible quantitative analyses in live imaging studies. Author summaryModern microscopy lets us watch living cells and embryos in three dimensions, but measuring brightness accurately is harder than it seems. Signals often become weaker not only when molecules are less abundant, but also when they lie deeper in the specimen or farther from the center of the image. This makes it difficult to tell whether differences in brightness reflect biology or simply the position of a cell within the microscope field. Existing correction methods typically rely on separately acquired reference measurement samples or on image-level statistical patterns. In this study, we took a different approach. Using the highly reproducible development of nematode (C. elegans) embryos, we compared cells that should be biologically equivalent across multiple embryos and used those repeated observations to estimate imaging bias directly from the biological images themselves. Our method corrects for both axial-dependent and radial attenuation simultaneously within a unified statistical framework, requiring no such reference data. Beyond simply improving consistency, we uncovered an unexpected result: the radial bias inferred from real embryos was opposite in sign to what calibration samples would predict. This underscores the need for specimen-specific, data-driven correction. Our framework should help make live imaging more quantitatively accurate for studying dynamic biological processes in complex three-dimensional specimens.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Ichihara, S., Akaho, S., Kuriki, S., Otomo, K., Nemoto, T., Kimura, A.. 2026-05-27. A Data-Driven Correction Framework for Axial- and Radial-Position-Dependent Intensity Attenuation in Volumetric Fluorescence Microscopy. https://doi.org/10.64898/2026.05.24.727559

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

Sequence context and partner availability specify divergent cell fates from a single transcription factor

Transcription factors drive the gene regulatory networks that control developmental transitions, yet which of their many targets a cell uses remains unresolved. Expressing Cebp, Cebp{beta} or Cebp{delta} identically, alone or with Oct4, Sox2, Klf4 and cMyc, gave four outcomes: adipocyte from fibroblasts and neural stem cells, trophectoderm from embryonic stem cells, and myeloid from B cells. Raising Cebp levels changed how many sites it reached, not which sequence it read: clustered motifs maintained somatic enhancers, while spillover onto low-copy sites created de novo enhancers carrying composites of Cebp and cell-type-restricted partners. In fibroblasts, Cebp also redistributed Oct4, Sox2 and Klf4 from early targets, blocking iPSC formation. Supplying the predicted partners rewrote the output: Spi1 redirected Cebp into parallel adipogenic and myeloid programs, via a transient PpargCD45 state using separate enhancers for each; TFAP2C abolished adipogenic conversion. Motif density and partner composites therefore assemble a factor's instructive output in the receiving cell.

cell biology↗

High-content screening identifies FDA-approved activators of mitophagy

Mitochondrial diseases are highly heterogeneous disorders caused by defects in oxidative phosphorylation, for which only limited therapeutic options are available. The elimination of dysfunctional mitochondria via mitophagy activation is an attractive strategy to treat several mitochondrial diseases, irrespective of the underlying genetic defect. To identify pharmacological activators of this pathway, we performed a high-content screening of 1,971 FDA-approved compounds using cellular reporters of TFEB nuclear translocation and mitophagy. This screening identified 294 compounds that promoted TFEB translocation, nine of which increased the number of mitolysosomes without compromising cell viability or damaging mitochondria. Among the selected compounds, Meptazinol and Ponatinib emerged as the top-ranked mitophagy inducers in fibroblasts from patients with complex I and IV deficiency, respectively, and were prioritised for further characterisation. However, they did not rescue the bioenergetic defect, suggesting that the stimulation of mitophagy per se is not sufficient to ameliorate the OXPHOS defect in mitochondrial diseases. Overall, our findings establish a scalable platform for the identification of pharmacological activators of TFEB and identify candidate compounds for therapeutic modulation of mitophagy.

cell biology↗

Matrix Gla Protein deficiency reveals a previously unrecognized mucosal calcification in the mouse airways

Tracheal calcification is a common finding that is considered to have limited clinical significance when detected most often in elderly individuals. Despite its frequent occurrence, the cellular and molecular mechanisms at the origin of tracheal calcification remain largely unexplored. In this context, we aimed to characterize the development of tracheal calcification, and to determine the role of matrix Gla protein (MGP), a major inhibitor of ectopic calcification whose genetic or pharmacologic deficiency is associated with premature tracheal calcification in humans. We found that wild-type mice undergo an unexpected early physiologic calcification of the tracheal cartilage rings beginning around one month after birth. This calcification progresses in a dynamic rostro-caudal sequence through a process involving terminal differentiation of tracheal chondrocytes. These findings challenge the prevailing view that tracheal cartilage is a permanent hyaline cartilage and instead reveals an early and highly organized physiologic calcification process. Furthermore, our findings further identify MGP as a key regulator of calcification within the respiratory tract. Indeed, MGP deficiency not only markedly accelerates tracheal cartilage calcification through a similar pattern and mechanism but also induces a previously unrecognized calcification of the tracheal mucosa, a lesion absent in wild-type mice. These alterations could partly explain the respiratory manifestations observed in MGP-deficient patients having Keutel syndrome, which include dyspnea, cough, stridor, and recurrent infections, symptoms previously being mainly attributed to calcification of the tracheal cartilage rings.

cell biology↗