Biology subjects

Kotz, M.

Publications and source records attributed to Kotz, M..

4 recordsLinked to original sources

bioRxiv2026

Contributions of human-caused climate change and individual emitters to global coral bleaching

Coral bleaching is among the most infamous climate impacts. Yet the extent of bleaching due to human-caused climate change, as opposed to natural El Nino variability, and the contributions of individual countries and carbon majors (fossil fuel and cement producers) remains unquantified. Here, we leverage coral monitoring globally across 4,479 sites from 1985-2024 to link specific emitters to marine heat stress and bleaching. For events with >10% of corals bleached at a site, we find that 99% (95% CI: 88-100%) were attributable to human-caused climate change. Even during major El Ninos, 97-100% of bleaching events were attributable to human-caused climate change and the extent of damage increases over time from 23% of sites bleached (95% CI: 3-35%) during 1998 to 71% of sites (95% CI: 37-85%) during 2023-2024. Emissions of the United States, the largest historical emitter, contributed to 51% (95% CI: 39-65%) of bleaching events. Emissions linked to Chevron, Saudi Aramco, Gazprom, and ExxonMobil each contributed to 14% (95% CI: 11-19%) of bleaching events -- roughly double the contribution of the 39 countries of the Alliance for Small Island States. It is virtually certain emissions of China, the United States, and Indonesia caused bleaching in their coastal waters. Strong inequalities exist where countries with high socioeconomic dependence on coral reefs experienced 54% of bleaching yet contributed only 5% to bleaching. As global warming rapidly nears levels catastrophic for warm-water corals, our results show the massive contribution from anthropogenic emissions to historical coral beaching and help fill an important evidentiary gap on accountability for non-economic loss and damage from climate change.

ecology↗

bioRxiv2026

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↗

bioRxiv2026

Programmable microactuators phase-lock cilia to local oscillatory flow

Hydrodynamic synchronization of motile cilia is essential for biological functions such as fluid transport, locomotion, and developmental patterning. It comprises the generation and the response to local flows in complex geometries. Besides their central role in physiology, direct experimental tests of ciliary responses to local flows at cellular length and time scales have remained elusive, largely due to the absence of tools capable of applying controlled, and localized flow stimuli. Here, we introduce programmable, nanometer-thin Ti/Pt microactuators that generate well-defined hydrodynamic forcing at biologically relevant frequencies while operating at biocompatible sub-Volt voltages. This platform is pioneering a controlled local hydrodynamic stimulation of individual motile cilia. We quantify the flow fields and forces produced by single microactuators using particle image velocimetry. Applying local oscillatory flows close to motile cilia of the green alga Chlamydomonas reinhardtii, we probe their dynamic response by quantifying phase-locking between cilia and microactuators. This quantification is aided by combining machine-learning-based image segmentation, oscillator phase reconstruction, and circular statistics. During actuation, we observe signatures of phase-locking: those include a reversible modulation of the fluctuations in phase-difference between cilium and actuator and a systematic shift in ciliary beating frequency. Beyond providing a bio-compatible and precise platform for local hydrodynamic stimulation, our approach establishes an experimental framework for directly testing theories of hydrodynamic synchronization and load adaptation in systems of motile cilia.

biophysics↗

bioRxiv2021

Identification of sex chromosomes using genomic and cytogenetic methods in a range-expanding spider, Argiope bruennichi (Araneae: Araneidae)

Differences between sexes in growth, ecology and behavior strongly shape species biology. In some animal groups, such as spiders, it is difficult or impossible to identify the sex of juveniles based on external morphology. This information would be useful for field surveys, behavioral experiments, and ecological studies on e.g. sex ratios and dispersal. In species with sex chromosomes, sex can be determined based on the specific sex chromosome complement. Additionally, information on the sequence of sex chromosomes provides the basis for studying sex chromosome evolution. We combined cytogenetic and genomic data to identify the sex chromosomes in the sexually dimorphic spider Argiope bruennichi, and designed RT-qPCR sex markers. We found that genome size and GC content of this spider falls into the range reported for the majority of araneids. The male karyotype is formed by 24 acrocentric chromosomes with an X1X20 sex chromosome system, with little similarity between X chromosomes, suggesting origin of these chromosomes by X chromosome fission or early duplication of an X chromosome and subsequent independent differentiation of the copies. Our data suggest similarly sized X chromosomes in A. bruennichi. They are smaller chromosomes of the complement. Our findings open the door to new directions in spider evolutionary and ecological research.

genetics↗