Biology subjects

Reichert, S.

Publications and source records attributed to Reichert, S..

4 recordsLinked to original sources

bioRxiv2026

Characterization of Vlf1 as a regulator of lipophagy.

Lipid droplets (LDs) are unique organelles, surrounded by a phospholipid monolayer. They are present in most eukaryotic cells including the unicellular model organism S. cerevisiae. LDs store neutral lipids which serve as precursors for amphipathic membrane lipids and as an energy reserve. Loss of LDs in S. cerevisiae results in multiple cellular defects impairing lipid homeostasis and the biogenesis and function of other organelles. Here, we find that the expression levels of many proteins in isolated mitochondrial fractions are altered in cells that cannot synthesize neutral lipids and therefore lack LDs. In addition, among several downregulated proteins, we identified the previously uncharacterized Ylr001c (which we name Vlf1 for Vacuolar Lipophagy Factor 1). We show that Vlf1 is glycosylated and, in contrast to some previous reports, is actually localized to the vacuole. Furthermore, we demonstrate that changes in Vlf1 expression alter growth sensitivity to rapamycin, and detected a physical interaction of Vlf1 with Atg15, a lipase involved in autophagy. Additionally, we observe higher levels of autophagy/lipophagy in the absence of Vlf1 and a reduction upon overexpression of the protein. Taken together, the effects on lipohagy by Vlf1 makes it, according to our knowledge, the first vacuolar lipophagy regulator identified in S. cerevisiae.

cell biology↗

bioRxiv2025

Motoneurons can count: A cell intrinsic spike number memory compensates for deviations from rate coding

Firing rate is an important means of encoding information in many types of neurons. A prime example is asynchronous flight as used by [~]600,000 insect species (Dudley, 2018), where wingbeat frequency and flight power output are controlled by a rate code of the flight power motoneurons (Hurkey et al., 2023). The five motoneurons that innervate the wing depressor muscle fibers translate different magnitudes of excitatory drive smoothly into changes of their common firing rates, which in turn, are linearly related to wing power output (Gordon and Dickinson, 2006). Such motoneuron input/output properties are called type-I excitability and are achieved by the expression of specific combinations of ion currents that linearize the frequency-input current curve. But are there additional motoneuron properties that compensate for acute perturbation of their rate code? Here we combine in vivo electrophysiology with Drosophila genetics to test for mechanisms that compensate for transient perturbation of rate coding during behavior. We show that MN intrinsic properties compensate for the occurrence of extra spikes by delaying the subsequent spikes, thus restoring rate coding fidelity. The underlying mechanism is dose and phase dependent. First, compensatory increases of subsequent interspike interval durations grow with the number of supernumerous spikes that interfere with coding. Second, the magnitude of the compensation for single extra spikes depends on when during an interspike interval these occur. This mechanism depends at least in part on axonally localized HCN channels and increases the fidelity of motoneuron rate coding in the light of perturbation during flight motor behavior.

neuroscience↗

bioRxiv2025

Warm and cool temperatures decrease early-life telomere length in wild pied flycatchers

Climate change represents a major challenge for avian species. It is characterized by an increase in average ambient temperatures, but also in occurrence of extreme weather events, such as heat weaves and cold snaps. These abrupt temperature changes can modify the immediate and long-term survival prospects of nestling birds, when their thermoregulatory capacities are still not fully developed. While immediate nestling survival can easily be measured, long-term survival is more challenging to evaluate. Early-life telomere length has been suggested as a potential biomarker of future fitness prospects. To evaluate the potential impact of changes in early-life temperature, we thus experimentally increased (ca. +2.8{degrees}C) and decreased (ca. -1.7{degrees}C) average nestbox temperatures in wild pied flycatchers (Ficedula hypoleuca) during nestling postnatal growth, and measured nestling telomere length before fledging. Shorter telomeres were observed in individuals exposed both to an experimental heating or cooling during growth. Our results suggest that long-term survival prospects or long-term performances of individuals exposed to abrupt changes in early-life temperature may be decreased. O_FIG O_LINKSMALLFIG WIDTH=197 HEIGHT=200 SRC="FIGDIR/small/651824v2_ufig1.gif" ALT="Figure 1"> View larger version (118K): org.highwire.dtl.DTLVardef@2ec526org.highwire.dtl.DTLVardef@915e9borg.highwire.dtl.DTLVardef@1da157borg.highwire.dtl.DTLVardef@b857ce_HPS_FORMAT_FIGEXP M_FIG C_FIG

zoology↗

bioRxiv2018

Neuronal activity drives homeostatic sleep through engagement of the hypothalamic neuropeptide galanin

Sleep pressure homeostatically increases during wake and dissipates during sleep, but the molecular signals and neuronal substrates that measure homeostatic sleep pressure remain poorly understood. A pharmacological assay that generates acute, short-term increases in wakefulness in larval zebrafish, revealed that subsequent rebound sleep is dependent on the intensity of global neuronal activity. Whole brain activity mapping identified preoptic Galanin expressing neurons as selectively active during rebound sleep, and the induction of galanin transcripts was predictive of total rebound sleep time. Galanin is required for sleep homeostasis, as galanin mutants almost completely lack rebound sleep following both pharmacologically induced neuronal activity and physical sleep deprivation. These results suggest that Galanin expressing neurons play a key role in integrating sleep pressure signals derived from global neuronal activity and act as an output arm for the vertebrate sleep homeostat. (word count: 129).

neuroscience↗