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Mateus, R.

Publications and source records attributed to Mateus, R..

4 recordsLinked to original sources

Developmental growth rates adapt to enable self-correction of organ morphology after injury.

Proportional organ growth requires tissue-level control of cell behavior. Yet the cues that adapt growth rates, especially after organ injury, remain unclear. Here, we uncover that developing organs are robust to extensive damage, triggering injury-specific mechanisms sufficient to override genetically-encoded size defects. Using precision microsurgery in developing zebrafish pectoral fins, we find that injury drives growth asynchronously across tissues and fin axes, by increasing proliferation and extracellular spacing. Growth compensation scales with the amount of tissue lost, restoring size and structure without compromising developmental timing. A feedback-control model captures these dynamics, suggesting that growth rates are regulated toward an organ-specific target area. At the molecular scale, injury signals bypass developmentally-regulated BMP gradient scaling. Injury instead activates de novo BMP signaling, which supports growth adaptation and rescues wildtype fin size in developmentally small mutants. Our findings identify an injury-dependent compensatory growth mechanism that resets developmental organ size, ensuring functional organ recovery.

developmental biology↗

GEQO biosensors for absolute analyte quantification in single cells

Genetically encoded fluorescent biosensors are widely used to monitor small molecule and ion levels in living cells. Quantitative FRET and FLIM sensors and highly sensitive intensiometric sensors have been developed for many analytes. Notwithstanding notable advances over the last years, a universal high-performance sensor design for absolute quantification that does not require specialized equipment has yet to be developed. We here report the GEQO platform of quantitative biosensors featuring calcium, ATP, cAMP, and organelle-specific variants. We used GEQO sensors to follow calcium and cAMP transients in immortalised cells, human pancreatic progenitor cells, and zebrafish embryos. We show that GEQO-based absolute quantification allows to account for analyte buffering and retains information in time trace data lost during relative quantification. GEQO biosensors will enable quantitative analyte measurements across a wide range of imaging platforms, a key prerequisite for diagnostic applications and quantitative approaches in basic cell biology.

cell biology↗

Injury-induced electrochemical coupling triggers regenerative cell proliferation

Organ injury triggers non-neuronal electric currents essential for regeneration. Yet, the mechanisms by which electrical signals are generated, sensed and transmitted upon damage to promote organ growth remain unclear. Here, we uncover that organ regeneration relies on dynamic electrochemical coupling between tissue-wide depolarization and intracellular proliferative signalling. By sub-second live imaging of injured zebrafish larval fins, we identify events across timescales: a millisecond tissue depolarization gradient, followed by seconds-persistent intracellular Calcium responses. Subsequently within one hour, Voltage Sensing Phosphatase activity translates depolarisation into proliferation. Connecting these timescales with an electro-diffusive model showed that ionic fluxes and electric potential become coupled in the fins interstitial space, enabling organ-wide signal spreading. Our work reveals the coupling between fast electrical signals and slower intracellular signalling, ensuring organ regeneration.

biophysics↗

The Role of Purine Interactions in Biogenic Crystal Shape Determination

Widespread through phyla, purine crystals are intracellular inclusions serving a myriad of organismal functions. In zebrafish, iridophores concentrate purines in membrane-bound organelles, the iridosomes, for controlled crystallization. These crystals assemble into large, flat, and thin hexagons following unknown mechanisms that evolve against thermodynamically favorable interactions. Here, we investigate the initial development of zebrafish iridosomal crystals. By performing in vivo confocal reflection imaging, cryoFIB-SEM, and establishing novel 2D and 3D analysis pipelines, we show that these crystals grow four times faster along the b-crystallographic axis, leading to their characteristic hexagonal shape. By analyzing zebrafish with impaired guanine production, while conducting crystal growth simulations, we find that crystal shape is directed by bond type, number, and interaction strength between purines. Mechanistically, the macroscopic shape of zebrafish crystals is controlled by the relative concentration of purines present in the iridosome. This process impacts crystal growth along the b-axis, by disrupting the crystals in-plane hydrogen bond structure, without alteration of the other axes. Our work uncovers a layer of biogenic crystal growth regulation occurring in vertebrate biocrystallization processes. HighlightsO_LIZebrafish iridophores actively regulate crystal size and shape within iridosomes C_LIO_LIIn vivo crystal (100) facet grows [~]4m{superscript 2} in 24 hours C_LIO_LILength of crystallographic b-axis is controlled by purine molecular interactions C_LIO_LISize of c- and a-axes is regulated independently of b-axis C_LI O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=180 SRC="FIGDIR/small/613275v1_ufig1.gif" ALT="Figure 1"> View larger version (46K): org.highwire.dtl.DTLVardef@1946819org.highwire.dtl.DTLVardef@3e6d34org.highwire.dtl.DTLVardef@737212org.highwire.dtl.DTLVardef@1462501_HPS_FORMAT_FIGEXP M_FIG C_FIG

biophysics↗