bioRxiv Science⌕ Search

Biology subjects

Batki, J.

Publications and source records attributed to Batki, J..

3 recordsLinked to original sources

SpinePy enables automated 3D spatiotemporal quantification of multicellular in vitro systems

Organoids and stem-cell-based embryo models such as gastruloids are powerful systems to quantitatively study morphogenesis and patterning. This requires 3D analysis in reference frames that emerge dynamically over development, but are less stereotypical than in vivo. Meaningful statistical comparison and interpretation of biological and physical quantities in space and time -- such as signaling activity, gene expression or cell flows -- depend on proper quantification in these internal and dynamic coordinate systems, especially in in vitro systems that naturally exhibit larger variation. Here, we present a computational framework, packaged as a modular Python toolkit termed SpinePy, that identifies the emergent primary body axis ("spine") of individual gastruloids and constructs a local, dynamic coordinate system aligned to their morphology. SpinePy enables 3D quantification relative to evolving axes and statistical comparisons of morphodynamics, patterning, and densities across structures with varying geometries. We validate and benchmark SpinePy using both synthetic and experimental gastruloid data, providing practical insights into method performance. Using this framework, we generate 3D patterning maps from gastruloids formed with different initial cell numbers (N0). This reveals distinct patterning classes that are better explained by gastruloid volumes than by N0. While demonstrated in gastruloids, SpinePy is broadly applicable to any multicellular system where analysis relative to evolving internal axes is needed, advancing quantitative and comparative spatial biology.

developmental biology↗

The molecular principles of Piwi-mediated co-transcriptional silencing through the dimeric SFiNX complex

Nuclear Argonaute proteins, guided to nascent target RNAs by their bound small RNAs, elicit co-transcriptional silencing through heterochromatin formation at transposon insertions and repetitive genomic loci. The molecular mechanisms involved in this process are incompletely understood. Here, we propose that the SFiNX complex, a silencing mediator downstream of nuclear Piwi-piRNA complexes in Drosophila, enables co-transcriptional silencing via the formation of molecular condensates. Condensate formation is stimulated by nucleic acid binding and requires SFiNX dimerization, mediated by the dynein light chain protein, LC8/Cutup. LC8s function within SFiNX can be bypassed with a heterologous dimerization domain, suggesting that dimerization is a constitutive feature of SFiNX. Mutations preventing LC8-mediated SFiNX dimerization result in loss of condensate formation in vitro and inability of Piwi to initiate heterochromatin formation and silence transposons in vivo. Formation of molecular condensates might be a general mechanism that underlies effective heterochromatin establishment at small RNA target loci in a co-transcriptional manner.

molecular biology↗

The nascent RNA binding complex SFiNX licenses piRNA-guided heterochromatin formation

The PIWI-interacting RNA (piRNA) pathway protects animal genome integrity in part through establishing repressive heterochromatin at transposon loci. Silencing requires piRNA-guided targeting of nuclear PIWI proteins to nascent transposon transcripts, yet the subsequent molecular events are not understood. Here, we identify SFiNX (Silencing Factor interacting Nuclear eXport variant), an interdependent protein complex required for Piwi-mediated co-transcriptional silencing in Drosophila. SFiNX consists of Nxf2-Nxt1, a gonad-specific variant of the heterodimeric mRNA export receptor Nxf1-Nxt1, and the Piwi-associated protein Panoramix. SFiNX mutant flies are sterile and exhibit transposon de-repression because piRNA-loaded Piwi is unable to establish heterochromatin. Within SFiNX, Panoramix recruits the heterochromatin effectors, while the RNA binding Nxf2 protein licenses co-transcriptional silencing. Our data reveal how Nxf2 evolved from an RNA transport receptor into a co-transcriptional silencing factor. Thus, NXF-variants, which are abundant in metazoans, can have diverse molecular functions and might have been co-opted for host genome defense more broadly.

molecular biology↗