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Hübner, S.

Publications and source records attributed to Hübner, S..

4 recordsLinked to original sources

A Locally Activatable Sensor for Robust Quantification of Organellar Glutathione

Glutathione (GSH) is the main determinant of intracellular redox potential and participates in multiple cellular signaling pathways. Achieving a detailed understanding of intracellular GSH trafficking and regulation depends on the development of tools to map GSH compartmentalization and intra-organelle fluctuations. Herein, we present a new GSH sensing platform, TRaQ-G, for live-cell imaging. This small-molecule/protein hybrid sensor possesses a unique reactivity turn-on mechanism that ensures that the small molecule is only sensitive to GSH in the desired location. Furthermore, TRaQ-G can be fused to a fluorescent protein of choice to give a ratiometric response. Using TRaQ-G-mGold, we demonstrated that the nuclear and cytosolic GSH pools are independently regulated during cell proliferation. We also used this sensor, in combination with roGFP, to quantify redox potential and GSH concentration simultaneously in the endoplasmic reticulum. Finally, by exchanging the fluorescent protein, we created a near-infrared, targetable and quantitative GSH sensor.

cell biology↗

Shift-inducible increase in recombination rate as an evolving strategy in a periodic environment: a numerical model

Numerous empirical studies have witnessed a plastic increase in meiotic recombination rate in organisms experiencing physiological stress due to unfavourable environmental conditions. Yet, it is not clear enough which characteristics of an ecological factor (intensity, duration, variability, etc.) make it stressogenic and therefore recombinogenic for an organism. Several previous theoretical models proceeded from the assumption that organisms increase their recombination rate when the environment becomes more severe, and demonstrated the evolutionary advantage of such recombination strategy. Here we explore another stress-associated recombination strategy, implying a reversible increase in recombination rate each time when the environment alternates. We allow such plastic changes in the organisms, grown in an environment different from that of their parents, and, optionally, also in their offspring. We show that such shift-inducible recombination is always favoured over intermediate constant optimal recombination. Besides, it sometimes outcompetes also zero and free optimal constant recombination, therefore making selection on recombination less polarized. Shift-inducible strategies with a longer, transgenerational plastic effect, are favoured under slightly stronger selection and longer period. These results hold for both panmixia and partial selfing, although selfing makes the dynamics of recombination modifier alleles faster. Our results suggest that epigenetic factors, presumably underlying the environmental plasticity of recombination, may play an important evolutionary role.

evolutionary biology↗

Fitness dependence preserves selection for recombination across diverse mixed mating systems

Meiotic recombination and the factors affecting its rate and fate in nature have inspired many theoretical studies in evolutionary biology. Classical theoretical models have inferred that non-zero recombination can be favoured under a rather restricted parameter range. Thus, the ubiquity of recombination in nature remains an open question. However, these models assumed constant (uniform) recombination with an equal rate across all individuals within the population. Models of fitness-dependent recombination, with the rate varying among genotypes according to their fitness have shown that such a strategy can often be favoured over the best constant recombination. Here we use simulations to show that across a range of mating systems with varying frequencies of selfing and clonality, fitness-dependent recombination is often favoured even when any non-zero constant recombination is disfavoured. This recombination-protecting effect of fitness dependence is strongest under intermediate rates of selfing or high rates of clonality.

evolutionary biology↗

On the origin of photoperiod non-responsiveness in barley

In barley, the transition from the vegetative to reproductive phase is complex and under the control of photoperiodic and temperature conditions. One major gene involved is PPD-H1, a PSEUDO-RESPONSE REGULATOR 7 (PRR7) that encodes a component of the circadian clock. Mutation at PPD-H1 resulted in the photoperiod non-responsive ppd-H1 alleles that are beneficial under high latitudinal environments as they allow vegetative growth during the long-day summer conditions whereby higher yields are harvested by farmers. Utilizing a diverse GWAS panel of world-wide origin and a genome-wide gene-based set of 50K SNP markers, a strong association of days to heading with the PPD-H1 gene was detected in multi-location field trials. Re-sequencing of the gene spanning putative causative SNPs, SNP22 (Turner et al. 2005) and SNP48 (Jones et al. 2008), detected recombination between the two, previously reported to be in complete LD. Phenotyping of the recombinants and phylogenetic relationships among haplotypes supported the original conclusion of Turner et al. (2005) that SNP22, present in the CCT domain, is the most likely causative SNP. To infer the origin of non-responsiveness, the PPD-H1 gene was re-sequenced in a geo-referenced collection of 2057 wild and domesticated barleys and compared with the allelic status of the 6000-year-old barley sample from the Yoram cave in the Masada cliff. A monophyletic and post-domestication origin in the Fertile Crescent was found in contrast to the pre-domestication origin proposed by Jones et al. (2008). We show that the photoperiod non-responsiveness originated from Desert type wild barley in the Southern Levant.Competing Interest StatementThe authors have declared no competing interest.View Full Text

plant biology↗