ResearchPad - 197 https://www.researchpad.co Default RSS Feed en-us © 2020 Newgen KnowledgeWorks <![CDATA[Phylogenetic clustering and rarity imply risk of local species extinction in prospective deep-sea mining areas of the Clarion–Clipperton Fracture Zone]]> https://www.researchpad.co/article/N01777460-8e8b-4c0c-b411-8f7e1d52e262 An understanding of the forces controlling community structure in the deep sea is essential at a time when its pristineness is threatened by polymetallic nodule mining. Because abiotically defined communities are more sensitive to environmental change, we applied occurrence- and phylogeny-based metrics to determine the importance of biotic versus abiotic structuring processes in nematodes, the most abundant invertebrate taxon of the Clarion–Clipperton Fracture Zone (CCFZ), an area targeted for mining. We investigated the prevalence of rarity and the explanatory power of environmental parameters with respect to phylogenetic diversity (PD). We found evidence for aggregation and phylogenetic clustering in nematode amplicon sequence variants (ASVs) and the dominant genus Acantholaimus, indicating the influence of environmental filtering, sympatric speciation, affinity for overlapping habitats and facilitation for community structure. PD was associated with abiotic variables such as total organic carbon, chloroplastic pigments equivalents and/or mud content, explaining up to 57% of the observed variability and providing further support of the prominence of environmental structuring forces. Rarity was high throughout, ranging from 64 to 75% unique ASVs. Communities defined by environmental filtering with a prevalence of rarity in the CCFZ suggest taxa of these nodule-bearing abyssal plains will be especially vulnerable to the risk of extinction brought about by the efforts to extract them.

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<![CDATA[Genetic architecture of a key reproductive isolation trait differs between sympatric and non-sympatric sister species of Lake Victoria cichlids]]> https://www.researchpad.co/article/Nd141aa0e-3c78-4fd4-aac5-04dac3d58edc One hallmark of the East African cichlid radiations is the rapid evolution of reproductive isolation that is robust to full sympatry of many closely related species. Theory predicts that species persistence and speciation in sympatry with gene flow are facilitated if loci of large effect or physical linkage (or pleiotropy) underlie traits involved in reproductive isolation. Here, we investigate the genetic architecture of a key trait involved in behavioural isolation, male nuptial coloration, by crossing two sister species pairs of Lake Victoria cichlids of the genus Pundamilia and mapping nuptial coloration in the F2 hybrids. One is a young sympatric species pair, representative of an axis of colour motif differentiation, red-dorsum versus blue, that is highly recurrent in closely related sympatric species. The other is a species pair representative of colour motifs, red-chest versus blue, that are common in allopatric but uncommon in sympatric closely related species. We find significant quantitative trait loci (QTLs) with moderate to large effects (some overlapping) for red and yellow in the sympatric red-dorsum × blue cross, whereas we find no significant QTLs in the non-sympatric red-chest × blue cross. These findings are consistent with theory predicting that large effect loci or linkage/pleiotropy underlying mating trait differentiation could facilitate speciation and species persistence with gene flow in sympatry.

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<![CDATA[Genetic affinity between Ningxia Hui and eastern Asian populations revealed by a set of InDel loci]]> https://www.researchpad.co/article/Naa3c2295-5c1b-4eaa-916f-9858243c3933

According to historical records, ethnic Hui in China obtained substantial genetic components from western Eurasian populations during their Islamization. However, some scholars believed that the ancestry of Hui people were native Chinese populations. In this context, the formation of Hui is due to simple cultural diffusion rather than demic diffusion. In this study, we examined the forensic and population genetic application of the 30 InDel loci in Hui population from Ningxia Hui Autonomous Region, Northwest China. Genotype analysis of 129 unrelated individuals revealed that all loci were in the Hardy–Weinberg equilibrium in Ningxia Hui. Forensic indices calculated from genotypes demonstrated that this panel, Qiagen DIPplex® Investigator kit, was powerful enough to be used in individual identification but not in paternity cases. Through population genetic analysis, we found that Ningxia Hui received much more genetic contributions from East Asian populations than those from western Eurasian populations. Finally, we statistically identified the admixture signal of eastern and western Eurasians, although the latter is weak, in Ningxia Hui via the three-population test. All this evidence suggested that the formation of Ningxia Hui was mainly attributed to the cultural transformation of local Chinese residents with minor gene flow from western Eurasian populations.

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<![CDATA[ALOX5, LPA, MMP9 and TPO gene polymorphisms increase atherothrombosis susceptibility in middle-aged Mexicans]]> https://www.researchpad.co/article/N98cfc2f6-fe5d-4021-932a-63ab53f12790

Atherothrombosis is the cornerstone of cardiovascular diseases and the primary cause of death worldwide. Genetic contribution to disturbances in lipid metabolism, coagulation, inflammation and oxidative stress increase the susceptibility to its development and progression. Given its multifactorial nature, the multiloci studies have been proposed as potential predictors of susceptibility. A cross-sectional study was conducted to explore the contribution of nine genes involved in oxidative stress, inflammatory and thrombotic processes in 204 subjects with atherothrombosis matched by age and gender with a healthy group (n = 204). To evaluate the possibility of spurious associations owing to the Mexican population genetic heterogeneity as well as its ancestral origins, 300 unrelated mestizo individuals and 329 Native Americans were also included. ALOX5, LPA, MMP9 and TPO gene polymorphisms, as well as their multiallelic combinations, were twice to four times more frequent in those individuals with clinical manifestations of atherothrombosis than in the healthy group. Once adjusting for population stratification was done, these differences remained. Our results add further evidence on the contribution of ALOX5, LPA, MMP9 and TPO polymorphisms to atherothrombosis development in the middle-aged group, emphasizing the multiethnic studies in search of gene risk polymorphisms.

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<![CDATA[Swimming exercise enhances brain plasticity in fish]]> https://www.researchpad.co/article/Ne006b784-5398-4813-a877-0df0b3599e8b

It is well-established that sustained exercise training can enhance brain plasticity and boost cognitive performance in mammals, but this phenomenon has not received much attention in fish. The aim of this study was to determine whether sustained swimming exercise can enhance brain plasticity in juvenile Atlantic salmon. Brain plasticity was assessed by both mapping the whole telencephalon transcriptome and conducting telencephalic region-specific microdissections on target genes. We found that 1772 transcripts were differentially expressed between the exercise and control groups. Gene ontology (GO) analysis identified 195 and 272 GO categories with a significant overrepresentation of up- or downregulated transcripts, respectively. A multitude of these GO categories was associated with neuronal excitability, neuronal signalling, cell proliferation and neurite outgrowth (i.e. cognition-related neuronal markers). Additionally, we found an increase in proliferating cell nuclear antigen (pcna) after both three and eight weeks of exercise in the equivalent to the hippocampus in fish. Furthermore, the expression of the neural plasticity markers synaptotagmin (syt) and brain-derived neurotrophic factor (bdnf) were also increased due to exercise in the equivalent to the lateral septum in fish. In conclusion, this is the first time that swimming exercise has been directly linked to increased telencephalic neurogenesis and neural plasticity in a teleost, and our results pave the way for future studies on exercise-induced neuroplasticity in fish.

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<![CDATA[Human transposon insertion profiling by sequencing (TIPseq) to map LINE-1 insertions in single cells]]> https://www.researchpad.co/article/N7337e351-b771-4063-ad2f-b2297370daf7

Long interspersed element-1 (LINE-1, L1) sequences, which comprise about 17% of human genome, are the product of one of the most active types of mobile DNAs in modern humans. LINE-1 insertion alleles can cause inherited and de novo genetic diseases, and LINE-1-encoded proteins are highly expressed in some cancers. Genome-wide LINE-1 mapping in single cells could be useful for defining somatic and germline retrotransposition rates, and for enabling studies to characterize tumour heterogeneity, relate insertions to transcriptional and epigenetic effects at the cellular level, or describe cellular phylogenies in development. Our laboratories have reported a genome-wide LINE-1 insertion site mapping method for bulk DNA, named transposon insertion profiling by sequencing (TIPseq). There have been significant barriers applying LINE-1 mapping to single cells, owing to the chimeric artefacts and features of repetitive sequences. Here, we optimize a modified TIPseq protocol and show its utility for LINE-1 mapping in single lymphoblastoid cells. Results from single-cell TIPseq experiments compare well to known LINE-1 insertions found by whole-genome sequencing and TIPseq on bulk DNA. Among the several approaches we tested, whole-genome amplification by multiple displacement amplification followed by restriction enzyme digestion, vectorette ligation and LINE-1-targeted PCR had the best assay performance.

This article is part of a discussion meeting issue ‘Crossroads between transposons and gene regulation’.

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<![CDATA[Transposable elements as a potent source of diverse cis-regulatory sequences in mammalian genomes]]> https://www.researchpad.co/article/N9ea8f7a1-a170-48c2-8302-884abaa3d683

Eukaryotic gene regulation is mediated by cis-regulatory elements, which are embedded within the vast non-coding genomic space and recognized by the transcription factors in a sequence- and context-dependent manner. A large proportion of eukaryotic genomes, including at least half of the human genome, are composed of transposable elements (TEs), which in their ancestral form carried their own cis-regulatory sequences able to exploit the host trans environment to promote TE transcription and facilitate transposition. Although not all present-day TE copies have retained this regulatory function, the preexisting regulatory potential of TEs can provide a rich source of cis-regulatory innovation for the host. Here, we review recent evidence documenting diverse contributions of TE sequences to gene regulation by functioning as enhancers, promoters, silencers and boundary elements. We discuss how TE-derived enhancer sequences can rapidly facilitate changes in existing gene regulatory networks and mediate species- and cell-type-specific regulatory innovations, and we postulate a unique contribution of TEs to species-specific gene expression divergence in pluripotency and early embryogenesis. With advances in genome-wide technologies and analyses, systematic investigation of TEs' cis-regulatory potential is now possible and our understanding of the biological impact of genomic TEs is increasing.

This article is part of a discussion meeting issue ‘Crossroads between transposons and gene regulation’.

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<![CDATA[Gene drive for population genetic control: non-functional resistance and parental effects]]> https://www.researchpad.co/article/N7498ff75-c52a-4894-ae77-5365b6eb19b4

Gene drive is a natural process of biased inheritance that, in principle, could be used to control pest and vector populations. As with any form of pest control, attention should be paid to the possibility of resistance evolving. For nuclease-based gene drive aimed at suppressing a population, resistance could arise by changes in the target sequence that maintain function, and various strategies have been proposed to reduce the likelihood that such alleles arise. Even if these strategies are successful, it is almost inevitable that alleles will arise at the target site that are resistant to the drive but do not restore function, and the impact of such sequences on the dynamics of control has been little studied. We use population genetic modelling of a strategy targeting a female fertility gene to demonstrate that such alleles may be expected to accumulate, and thereby reduce the reproductive load on the population, if nuclease expression per se causes substantial heterozygote fitness effects or if parental (especially paternal) deposition of nuclease either reduces offspring fitness or affects the genotype of their germline. All these phenomena have been observed in synthetic drive constructs. It will, therefore, be important to allow for non-functional resistance alleles in predicting the dynamics of constructs in cage populations and the impacts of any field release.

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<![CDATA[A method yielding comparable estimates of the fraternal birth order and female fecundity effects in male homosexuality]]> https://www.researchpad.co/article/N23d37b70-3e88-441d-b53c-b177edd61a25

The fraternal birth order effect (FBOE) is the finding that older brothers increase the probability of homosexuality in later-born males, and the female fecundity effect (FFE) is the finding that the mothers of homosexual males produce more offspring than the mothers of heterosexual males. In a recent paper, Khovanova proposed a novel method for computing independent estimates of these effects on the same samples and expressing the magnitude and direction of the effects in the same metric. In her procedure, only families with one or two sons are examined, and daughters are ignored. The present study investigated the performance of Khovanova's method using archived data from 10 studies, comprising 14 samples totalling 5390 homosexual and heterosexual subjects. The effect estimate for the FBOE showed that an increase from zero older brothers to one older brother is associated with a 38% increase in the odds of homosexuality. By contrast, the effect estimate for the FFE showed that the increase from zero younger brothers to one younger brother is not associated with any increase in the odds of homosexuality. The former result supports the maternal immune hypothesis of male homosexuality; the latter result does not support the balancing selection hypothesis.

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<![CDATA[Nutritional regulation of glucose metabolism-related genes in the emerging teleost model Mexican tetra surface fish: a first exploration]]> https://www.researchpad.co/article/N76605add-50ae-427b-a82c-74d849d88c91

Astyanax mexicanus has gained importance as a laboratory model organism for evolutionary biology. However, little is known about its intermediary metabolism, and feeding regimes remain variable between laboratories holding this species. We thus aimed to evaluate the intermediary metabolism response to nutritional status and to low (NC) or high (HC) carbohydrate diets in various organs of the surface-dwelling form of the species. As expected, glycaemia increased after feeding. Fish fed the HC diet had higher glycaemia than fish fed the NC diet, but without displaying hyperglycaemia, suggesting that carbohydrates are efficiently used as an energy source. At molecular level, only fasn (Fatty Acid Synthase) transcripts increased in tissues after refeeding, suggesting an activation of lipogenesis. On the other hand, we monitored only moderate changes in glucose-related transcripts. Most changes observed were related to the nutritional status, but not to the NC versus HC diet. Such a metabolic pattern is suggestive of an omnivorous-related metabolism, and this species, at least at adult stage, may adapt to a fish meal-substituted diet with high carbohydrate content and low protein supply. Investigation to identify molecular actors explaining the efficient use of such a diet should be pursued to deepen our knowledge on this species.

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<![CDATA[Correction to ‘ALOX5, LPA, MMP9 and TPO gene polymorphisms increase atherothrombosis susceptibility in middle-aged Mexicans’]]> https://www.researchpad.co/article/N267030b5-01c8-4096-af52-adcd5097a8e5 ]]> <![CDATA[On the relations of phase separation and Hi-C maps to epigenetics]]> https://www.researchpad.co/article/N9d79cf97-4f2a-41bc-82e3-692014a66984

The relationship between compartmentalization of the genome and epigenetics is long and hoary. In 1928, Heitz defined heterochromatin as the largest differentiated chromatin compartment in eukaryotic nuclei. Müller's discovery of position-effect variegation in 1930 went on to show that heterochromatin is a cytologically visible state of heritable (epigenetic) gene repression. Current insights into compartmentalization have come from a high-throughput top-down approach where contact frequency (Hi-C) maps revealed the presence of compartmental domains that segregate the genome into heterochromatin and euchromatin. It has been argued that the compartmentalization seen in Hi-C maps is owing to the physiochemical process of phase separation. Oddly, the insights provided by these experimental and conceptual advances have remained largely silent on how Hi-C maps and phase separation relate to epigenetics. Addressing this issue directly in mammals, we have made use of a bottom-up approach starting with the hallmarks of constitutive heterochromatin, heterochromatin protein 1 (HP1) and its binding partner the H3K9me2/3 determinant of the histone code. They are key epigenetic regulators in eukaryotes. Both hallmarks are also found outside mammalian constitutive heterochromatin as constituents of larger (0.1–5 Mb) heterochromatin-like domains and smaller (less than 100 kb) complexes. The well-documented ability of HP1 proteins to function as bridges between H3K9me2/3-marked nucleosomes contributes to polymer–polymer phase separation that packages epigenetically heritable chromatin states during interphase. Contacts mediated by HP1 ‘bridging’ are likely to have been detected in Hi-C maps, as evidenced by the B4 heterochromatic subcompartment that emerges from contacts between large KRAB-ZNF heterochromatin-like domains. Further, mutational analyses have revealed a finer, innate, compartmentalization in Hi-C experiments that probably reflect contacts involving smaller domains/complexes. Proteins that bridge (modified) DNA and histones in nucleosomal fibres—where the HP1–H3K9me2/3 interaction represents the most evolutionarily conserved paradigm—could drive and generate the fundamental compartmentalization of the interphase nucleus. This has implications for the mechanism(s) that maintains cellular identity, be it a terminally differentiated fibroblast or a pluripotent embryonic stem cell.

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<![CDATA[European and Asian contribution to the genetic diversity of mainland South American chickens]]> https://www.researchpad.co/article/Ncda79dac-9268-47ad-b5cd-3f251554dabe

Chickens (Gallus gallus domesticus) from the Americas have long been recognized as descendants of European chickens, transported by early Europeans since the fifteenth century. However, in recent years, a possible pre-Columbian introduction of chickens to South America by Polynesian seafarers has also been suggested. Here, we characterize the mitochondrial control region genetic diversity of modern chicken populations from South America and compare this to a worldwide dataset in order to investigate the potential maternal genetic origin of modern-day chicken populations in South America. The genetic analysis of newly generated chicken mitochondrial control region sequences from South America showed that the majority of chickens from the continent belong to mitochondrial haplogroup E. The rest belongs to haplogroups A, B and C, albeit at very low levels. Haplogroup D, a ubiquitous mitochondrial lineage in Island Southeast Asia and on Pacific Islands is not observed in continental South America. Modern-day mainland South American chickens are, therefore, closely allied with European and Asian chickens. Furthermore, we find high levels of genetic contributions from South Asian chickens to those in Europe and South America. Our findings demonstrate that modern-day genetic diversity of mainland South American chickens appear to have clear European and Asian contributions, and less so from Island Southeast Asia and the Pacific Islands. Furthermore, there is also some indication that South Asia has more genetic contribution to European chickens than any other Asian chicken populations.

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<![CDATA[A practical view of fine-mapping and gene prioritization in the post-genome-wide association era]]> https://www.researchpad.co/article/N8e494b47-64da-4604-aa32-679a75731a0f

Over the past 15 years, genome-wide association studies (GWASs) have enabled the systematic identification of genetic loci associated with traits and diseases. However, due to resolution issues and methodological limitations, the true causal variants and genes associated with traits remain difficult to identify. In this post-GWAS era, many biological and computational fine-mapping approaches now aim to solve these issues. Here, we review fine-mapping and gene prioritization approaches that, when combined, will improve the understanding of the underlying mechanisms of complex traits and diseases. Fine-mapping of genetic variants has become increasingly sophisticated: initially, variants were simply overlapped with functional elements, but now the impact of variants on regulatory activity and direct variant-gene 3D interactions can be identified. Moreover, gene manipulation by CRISPR/Cas9, the identification of expression quantitative trait loci and the use of co-expression networks have all increased our understanding of the genes and pathways affected by GWAS loci. However, despite this progress, limitations including the lack of cell-type- and disease-specific data and the ever-increasing complexity of polygenic models of traits pose serious challenges. Indeed, the combination of fine-mapping and gene prioritization by statistical, functional and population-based strategies will be necessary to truly understand how GWAS loci contribute to complex traits and diseases.

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<![CDATA[A kinase of many talents: non-neuronal functions of CDK5 in development and disease]]> https://www.researchpad.co/article/Nd385aeb5-41de-456c-98d6-b958095d21f3

The cyclin-dependent kinase 5 (CDK5) represents an unusual member of the family of cyclin-dependent kinases, which is activated upon binding to non-cyclin p35 and p39 proteins. The role of CDK5 in the nervous system has been very well established. In addition, there is growing evidence that CDK5 is also active in non-neuronal tissues, where it has been postulated to affect a variety of functions such as the immune response, angiogenesis, myogenesis, melanogenesis and regulation of insulin levels. Moreover, high levels of CDK5 have been observed in different tumour types, and CDK5 was proposed to play various roles in the tumorigenic process. In this review, we discuss these various CDK5 functions in normal physiology and disease, and highlight the therapeutic potential of targeting CDK5.

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<![CDATA[Heritability and genetic correlations of personality, life history and morphology in the grey mouse lemur (Microcebus murinus)]]> https://www.researchpad.co/article/Nf7ae2c31-d771-4054-b17d-fd5a2c6f1f2e

The recent interest in animal personality has sparked a number of studies on the heritability of personality traits. Yet, how the sources variance these traits can be decomposed remains unclear. Moreover, whether genetic correlations with life-history traits, personality traits and other phenotypic traits exist as predicted by the pace-of-life syndrome hypothesis remains poorly understood. Our aim was to compare the heritability of personality, life-history and morphological traits and their potential genetic correlations in a small primate (Microcebus murinus). We performed an animal model analysis on six traits measured in a large sample of captive mouse lemurs (N = 486). We chose two personality traits, two life-history traits and two morphological traits to (i) estimate the genetic and/or environmental contribution to their variance, and (ii) test for genetic correlations between these traits. We found modest narrow-sense heritability for personality traits, morphological traits and life-history traits. Other factors including maternal effects also influence the sources of variation in life-history and morphological traits. We found genetic correlations between emergence latency on the one hand and radius length and growth rate on the other hand. Emergence latency was also genetically correlated with birth weight and was influenced by maternal identity. These results provide insights into the influence of genes and maternal effects on the partitioning of sources of variation in personality, life-history and morphological traits in a captive primate model and suggest that the pace-of-life syndrome may be partly explained by genetic trait covariances.

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<![CDATA[Inferring Atlantic salmon post-smolt migration patterns using genetic assignment]]> https://www.researchpad.co/article/Nd49a170c-204d-4a17-bf51-56b17a68e128

Understanding migratory patterns is important for predicting and mitigating unwanted consequences of environmental change or anthropogenic challenges on vulnerable species. Wild Atlantic salmon undergo challenging migrations between freshwater and marine environments, and the numbers of salmon returning to their natal rivers to reproduce have declined over several decades. Mortality from sea lice linked to fish farms within their seaward migration routes is proposed as a contributing factor to these declines. Here, we used 31 microsatellite markers to establish a genetic baseline for the main rivers in the Hardangerfjord, western Norway. Mixed stock analysis was used to assign Atlantic salmon post-smolts caught in trawls in 2013–2017 back to regional reporting units. Analyses demonstrated that individuals originating from rivers located in the inner region of the fjord arrived at the outer fjord later than individuals from middle and outer fjord rivers. Therefore, as post-smolts originating from inner rivers also have to migrate longer distances to exit the fjord, these data suggest that inner fjord populations are more likely to be at risk of mortality through aquaculture-produced sea lice, and other natural factors such as predation, than middle or outer fjord populations with earlier exit times and shorter journeys. These results will be used to calibrate models estimating mortality from sea lice on wild salmon for the regulation of the Norwegian aquaculture industry.

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<![CDATA[DNA damage responses in ageing]]> https://www.researchpad.co/article/N9ba2797f-4e75-45c8-9a1b-e41c87fe3782

Ageing appears to be a nearly universal feature of life, ranging from unicellular microorganisms to humans. Longevity depends on the maintenance of cellular functionality, and an organism's ability to respond to stress has been linked to functional maintenance and longevity. Stress response pathways might indeed become therapeutic targets of therapies aimed at extending the healthy lifespan. Various progeroid syndromes have been linked to genome instability, indicating an important causal role of DNA damage accumulation in the ageing process and the development of age-related pathologies. Recently, non-cell-autonomous mechanisms including the systemic consequences of cellular senescence have been implicated in regulating organismal ageing. We discuss here the role of cellular and systemic mechanisms of ageing and their role in ageing-associated diseases.

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<![CDATA[mastermind regulates niche ageing independently of the Notch pathway in the Drosophila ovary]]> https://www.researchpad.co/article/N040fee86-90db-4469-b8a0-4bb12e155bde

Proper stem cell activity in tissues ensures the correct balance between proliferation and differentiation, thus allowing tissue homeostasis and repair. The Drosophila ovary develops well-defined niches that contain on average 2–4 germline stem cells (GSCs), whose maintenance depends on systemic signals and local factors. A known player in the decline of tissue homeostasis is ageing, which correlates with the waning of resident stem cell populations. In Drosophila, ovaries from old females contain fewer GSCs than those from young flies. We isolated niche cells of aged ovaries, performed a transcriptomic analysis and identified mastermind (mam) as a factor for Drosophila ovarian niche functionality during ageing. We show that mam is upregulated in aged niche cells and that we can induce premature GSC loss by overexpressing mam in otherwise young niche cells. High mam levels in niche cells induce reduced Hedgehog amounts, a decrease in cadherin levels and a likely increase in reactive oxygen species, three scenarios known to provoke GSC loss. Mam is a canonical co-activator of the Notch pathway in many Drosophila tissues. However, we present evidence to support a Notch-independent role for mam in the ovarian germline niche.

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<![CDATA[Consequences of past climate change and recent human persecution on mitogenomic diversity in the arctic fox]]> https://www.researchpad.co/article/Ne80d7618-c81f-46cb-8339-2b6e217d69dd

Ancient DNA provides a powerful means to investigate the timing, rate and extent of population declines caused by extrinsic factors, such as past climate change and human activities. One species probably affected by both these factors is the arctic fox, which had a large distribution during the last glaciation that subsequently contracted at the start of the Holocene. More recently, the arctic fox population in Scandinavia went through a demographic bottleneck owing to human persecution. To investigate the consequences of these processes, we generated mitogenome sequences from a temporal dataset comprising Pleistocene, historical and modern arctic fox samples. We found no evidence that Pleistocene populations in mid-latitude Europe or Russia contributed to the present-day gene pool of the Scandinavian population, suggesting that postglacial climate warming led to local population extinctions. Furthermore, during the twentieth-century bottleneck in Scandinavia, at least half of the mitogenome haplotypes were lost, consistent with a 20-fold reduction in female effective population size. In conclusion, these results suggest that the arctic fox in mainland Western Europe has lost genetic diversity as a result of both past climate change and human persecution. Consequently, it might be particularly vulnerable to the future challenges posed by climate change.

This article is part of a discussion meeting issue ‘The past is a foreign country: how much can the fossil record actually inform conservation?’

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