scholarly journals Nongenetic inheritance and multigenerational plasticity in the nematode C. elegans

eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
L Ryan Baugh ◽  
Troy Day
Keyword(s):  
Phenotypic Plasticity ◽  
Model Systems ◽  
Future Research ◽  
Cellular Mechanisms ◽  
Adaptive Changes ◽  
Multiple Generations ◽  
C Elegans ◽  
Evolutionary Thought ◽  
Growing Body ◽  
Nongenetic Inheritance

A rapidly growing body of literature in several organisms suggests that environmentally-induced adaptive changes in phenotype can be transmitted across multiple generations. Although within-generation plasticity has been well documented, multigenerational plasticity represents a significant departure from conventional evolutionary thought. Studies of C. elegans have been particularly influential because this species exhibits extensive phenotypic plasticity, it is often essentially isogenic, and it has well-documented molecular and cellular mechanisms through which nongenetic inheritance occurs. However, while experimentalists are eager to claim that nongenetic modes of inheritance characterized in this and other model systems enhance fitness, many biologists remain skeptical given the extraordinary nature of this claim. We establish three criteria to evaluate how compelling the evidence for adaptive multigenerational plasticity is, and we use these criteria to critically examine putative cases of it in C. elegans. We conclude by suggesting potentially fruitful avenues for future research.

scholarly journals Crosstalk between Different DNA Repair Pathways Contributes to Neurodegenerative Diseases

Biology ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 163
Author(s):  
Swapnil Gupta ◽  
Panpan You ◽  
Tanima SenGupta ◽  
Hilde Nilsen ◽  
Kulbhushan Sharma
Keyword(s):  
Dna Repair ◽  
Neurodegenerative Diseases ◽  
3D Models ◽  
Model Systems ◽  
Spinocerebellar Ataxias ◽  
C Elegans ◽  
Cellular Processes ◽  
Age Related ◽  
Damage Response ◽  
Lateral Sclerosis

Genomic integrity is maintained by DNA repair and the DNA damage response (DDR). Defects in certain DNA repair genes give rise to many rare progressive neurodegenerative diseases (NDDs), such as ocular motor ataxia, Huntington disease (HD), and spinocerebellar ataxias (SCA). Dysregulation or dysfunction of DDR is also proposed to contribute to more common NDDs, such as Parkinson’s disease (PD), Alzheimer’s disease (AD), and Amyotrophic Lateral Sclerosis (ALS). Here, we present mechanisms that link DDR with neurodegeneration in rare NDDs caused by defects in the DDR and discuss the relevance for more common age-related neurodegenerative diseases. Moreover, we highlight recent insight into the crosstalk between the DDR and other cellular processes known to be disturbed during NDDs. We compare the strengths and limitations of established model systems to model human NDDs, ranging from C. elegans and mouse models towards advanced stem cell-based 3D models.

scholarly journals SEM and TEM for identification of capsular fibrosis and cellular behavior around breast implants – a descriptive analysis

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Britta Kuehlmann ◽  
Isabel Zucal ◽  
Clark Andrew Bonham ◽  
Lydia-Marie Joubert ◽  
Lukas Prantl
Keyword(s):  
Descriptive Analysis ◽  
Breast Implants ◽  
Foreign Body Response ◽  
Future Research ◽  
Cellular Mechanisms ◽  
Tem Analysis ◽  
Capsular Fibrosis ◽  
Sem And Tem ◽  
Post Operation ◽  
Bacterial Accumulation

Abstract Background Capsular fibrosis (CF) is the most common long-term complication in implant-based breast augmentation. It is well accepted that the foreign body response (FBR) instigates the development of fibrotic disease. Our study aims to compare murine and human samples of CF and describe the cellular and extracellular matrix (ECM) composition using scanning and transmission electron microscopy (SEM and TEM). Results Miniature microtextured silicone breast implants were implanted in mice and subsequently harvested at days 15, 30, and 90 post-operation. Isolated human capsules with the most aggravated form of CF (Baker IV) were harvested post-operation. Both were analyzed with SEM and TEM to assess cellular infiltration and ECM structure. An architectural shift of collagen fiber arrangement from unidirectional to multidirectional was observed at day 90 when compared to days 15 and 30. Fibrosis was observed with an increase of histiocytic infiltration. Moreover, bacterial accumulation was seen around silicone fragments. These findings were common in both murine and human capsules. Conclusions This murine model accurately recapitulates CF found in humans and can be utilized for future research on cellular invasion in capsular fibrosis. This descriptive study helps to gain a better understanding of cellular mechanisms involved in the FBR. Increases of ECM and cellularity were observed over time with SEM and TEM analysis.

A Cuticle Collagen Encoded by the lon-3 Gene May Be a Target of TGF-β Signaling in Determining Caenorhabditis elegans Body Shape

Genetics ◽  
2002 ◽  
Vol 162 (4) ◽  
pp. 1631-1639
Author(s):  
Yo Suzuki ◽  
Gail A Morris ◽  
Min Han ◽  
William B Wood
Keyword(s):  
Caenorhabditis Elegans ◽  
Body Shape ◽  
Small Body ◽  
Dependent Manner ◽  
Loss Of Function ◽  
Cellular Mechanisms ◽  
C Elegans ◽  
Gene Expression Analyses ◽  
Dose Dependent

Abstract The signaling pathway initiated by the TGF-β family member DBL-1 in Caenorhabditis elegans controls body shape in a dose-dependent manner. Loss-of-function (lf) mutations in the dbl-1 gene cause a short, small body (Sma phenotype), whereas overexpression of dbl-1 causes a long body (Lon phenotype). To understand the cellular mechanisms underlying these phenotypes, we have isolated suppressors of the Sma phenotype resulting from a dbl-1(lf) mutation. Two of these suppressors are mutations in the lon-3 gene, of which four additional alleles are known. We show that lon-3 encodes a collagen that is a component of the C. elegans cuticle. Genetic and reporter-gene expression analyses suggest that lon-3 is involved in determination of body shape and is post-transcriptionally regulated by the dbl-1 pathway. These results support the possibility that TGF-β signaling controls C. elegans body shape by regulating cuticle composition.

scholarly journals Rictor/TORC2 mediates gut-to-brain signaling in the regulation of phenotypic plasticity in C. elegans

PLoS Genetics ◽  
2018 ◽  
Vol 14 (2) ◽  
pp. e1007213 ◽  
Author(s):  
Michael P. O’Donnell ◽  
Pin-Hao Chao ◽  
Jan E. Kammenga ◽  
Piali Sengupta
Keyword(s):  
Phenotypic Plasticity ◽  
C Elegans

A systematic review of constructive and solutions journalism research

Journalism ◽  
2021 ◽  
pp. 146488492110445
Author(s):  
Kyser Lough ◽  
Karen McIntyre
Keyword(s):  
Systematic Review ◽  
The State ◽  
Future Research ◽  
Academic Activity ◽  
Growing Body ◽  
The Future ◽  
Solutions Journalism ◽  
Journalism Research ◽  
Constructive Journalism

Academic activity surrounding constructive and solutions journalism has surged in recent years; thus, it is important to pause and reflect on this growing body of work in order to understand where the field can and should go in the future. We conducted a systematic review of existing literature on solutions and constructive journalism ( N = 94), in an effort to (1) describe the state of this field by identifying the patterns and trends in the methodological and conceptual approaches, topics, institutions, countries and practices involved in this research, and (2) illuminate potentially important gaps in the field and suggest recommendations for future research.

Abstract 5402: Two Photon Microscopy Measurements Of Sub-epicardial Sarcomere Length In Perfused Rat Hearts

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Patrizia Camelliti ◽  
Gil Bub ◽  
Daniel J Stuckey ◽  
Christian Bollensdorff ◽  
Damian J Tyler ◽  
...  
Keyword(s):  
Sarcomere Length ◽  
Left Ventricular ◽  
Model Systems ◽  
Future Research ◽  
Fundamental Parameter ◽  
Rat Hearts ◽  
Perfused Hearts ◽  
Over Time

Sarcomere length (SL) is a fundamental parameter underlying the Frank Starling relation in the heart, as it offers an absolute representation of myocardial stretch. Previous studies addressed the Frank Starling relation by measuring SL in isolated myocytes or muscle strips. Here, we report first data obtained using a novel technique to measure sub-epicardial SL in perfused hearts. Rat hearts were Langendorff perfused (normal Tyrode solution) at a constant pressure of 90mmHg, labeled with the fluorescent membrane marker di-4-ANEPPS, and then arrested with high-K + Tyrode for either 2-photon microscopy (n=4) or MRI (n=4). Image analysis software was developed to extract SL at the cell level from >1,400 2-photon images (Fig 1 ) and correct for cell angle. SL increased by 10±2 % between 30 and 80 min of perfusion (1.98±0.04 to 2.17±0.03 μm; p<0.05; Fig 1 ). Measurements of left ventricular myocardial volume (LVMV) were made in vivo and in perfused hearts using 3D MRI. LVMV increased by 24±7% from in vivo to 30 min of perfusion, and by 11±3 % between 30 and 90 min (539±35; 664±44; 737±49 mm 3 , respectively; p<0.05; Fig 1 ). We show that SL can be measured in isolated perfused hearts. The method allowed monitoring of changes in SL over time, and showed that SL and LVMV increase to a similar extent during 30–80 min perfusion with crystalloid solution, probably due to tissue oedema. This result, together with the increase in LVMV during the first 30 min, highlights the pronounced differences between in vivo , in situ , and in vitro model systems for studies of cardiac physiology and mechanics. Future research will compare changes in SL in healthy hearts and disease models involving contractile dysfunction. Figure 1: Left: 2-photon microscopy image of di-4-ANEPPS labeled myocardium. Right: SL and LVMV changes over time.

scholarly journals Birds facing climate change: a qualitative model for the adaptive potential of migratory behaviour

2015 ◽  
Vol 85 (1) ◽  
pp. 3 ◽  
Author(s):  
Michelangelo Morganti
Keyword(s):  
Climate Change ◽  
Phenotypic Plasticity ◽  
Migratory Birds ◽  
Future Research ◽  
Qualitative Model ◽  
Migratory Behaviour ◽  
Adaptive Potential ◽  
Long Distance ◽  
Genetic Determination ◽  
Recent Climate

Recent climate change is altering the migratory behaviour of many bird species. An advancement in the timing of spring events and a shift in the geographical distribution have been detected for birds around the world. In particular, intra-Palearctic migratory birds have advanced arrivals in spring and shortened migratory distances by shifting northward their wintering grounds. These changes in migratory patterns are considered adaptive responses facilitating the adjustment of the life cycle to the phenological changes found in their breeding areas. However, in some cases, populations exposed to the same selective pressures do not show any appreciable adaptive change in their behaviour. Basing on the comparison of realized and non-realized adaptive changes, I propose here the formulation of a qualitative model that predicts the potential of migratory birds populations to change adaptively their migratory behaviour. The model assumes that the adaptive potential of migratory behaviour is fuelled by both genetic diversity and phenotypic plasticity. Populations of long-distance migrants are exposed to strong environmental canalization that largely eroded their phenotypic plasticity and reduced genetic variability, so that they show a very low amount of adaptive potential regarding migratory behaviour. On the contrary, partial-migrant populations have a highly varied genetic profile and are more plastic at the phenotypic level, and consequently show the highest amount of adaptive potential. Species with mainly social and mainly genetic determination of the migratory behaviour are separately treated in the model. Specific empirical models to foresee the adaptive strategies of wild bird populations that face to climate change can be derived from the general theoretical model. As example, a specific model about the shortening of migratory distances in Western European migratory bird is presented. Finally, a number of future research lines on the topic of adaptive potential of migratory behaviour are discussed, including some examples of concrete study cases. In conclusion, partial-migration emerge as the less known system and future research efforts on this topic are expected to be especially fruitful.

scholarly journals Graptopetalum paraguayense Extract Ameliorates Proteotoxicity in Aging and Age-Related Diseases in Model Systems

Nutrients ◽  
2021 ◽  
Vol 13 (12) ◽  
pp. 4317
Author(s):  
Yan-Xi Chen ◽  
Phuong Thu Nguyen Le ◽  
Tsai-Teng Tzeng ◽  
Thu-Ha Tran ◽  
Anh Thuc Nguyen ◽  
...  
Keyword(s):  
Model Systems ◽  
Wild Type ◽  
Nematode Caenorhabditis Elegans ◽  
Cancer Cell Growth ◽  
C Elegans ◽  
Age Related ◽  
Ampk Activity ◽  
Β Amyloid ◽  
Amp Activated Protein Kinase ◽  
U87 Cells

Declines in physiological functions are the predominant risk factors for age-related diseases, such as cancers and neurodegenerative diseases. Therefore, delaying the aging process is believed to be beneficial in preventing the onset of age-related diseases. Previous studies have demonstrated that Graptopetalum paraguayense (GP) extract inhibits liver cancer cell growth and reduces the pathological phenotypes of Alzheimer’s disease (AD) in patient IPS-derived neurons. Here, we show that GP extract suppresses β-amyloid pathology in SH-SYS5Y-APP695 cells and APP/PS1 mice. Moreover, AMP-activated protein kinase (AMPK) activity is enhanced by GP extract in U87 cells and APP/PS1 mice. Intriguingly, GP extract enhances autophagy in SH-SYS5Y-APP695 cells, U87 cells, and the nematode Caenorhabditis elegans, suggesting a conserved molecular mechanism by which GP extract might regulate autophagy. In agreement with its role as an autophagy activator, GP extract markedly diminishes mobility decline in polyglutamine Q35 mutants and aged wild-type N2 animals in C. elegans. Furthermore, GP extract significantly extends lifespan in C. elegans.

scholarly journals The genetic paradigms of dietary restriction fail to extend life span in cep-1(gk138) mutant of C. elegans p53 due to possible background mutations

2020 ◽  
Author(s):  
Anita Goyala ◽  
Aiswarya Baruah ◽  
Arnab Mukhopadhyay
Keyword(s):  
Life Span ◽  
Dietary Restriction ◽  
Model Systems ◽  
Regulation Of Expression ◽  
Life Span Extension ◽  
Phenotypic Differences ◽  
C Elegans ◽  
Xenobiotic Detoxification ◽  
Organismal Biology ◽  
Extend Life Span

AbstractDietary restriction (DR) increases life span and improves health in most model systems tested, including non-human primates. In C. elegans, as in other models, DR leads to reprogramming of metabolism, improvements in mitochondrial health, large changes in gene expression, including increase in expression of cytoprotective genes, better proteostasis etc. Understandably, multiple global transcriptional regulators like transcription factors FOXO/DAF-16, FOXA/PHA-4, HSF1/HSF-1 and NRF2/SKN-1 are important for DR longevity. Considering the wide-ranging effects of p53 on organismal biology, we asked whether the C. elegans ortholog, CEP-1 is required for DR-mediated longevity assurance. We employed the widely-used TJ1 strain of cep-1(gk138). We show that cep-1(gk138) suppresses the life span extension of two genetic paradigms of DR, but two non-genetic modes of DR remain unaffected in this strain. We find that in cep-1(gk138), two aspects of DR, increased autophagy and the up-regulation of expression of cytoprotective xenobiotic detoxification program (cXDP) genes are dampened. Importantly, we find that background mutation(s) in the strain may be the actual cause for the phenotypic differences that we observed and cep-1 may not be directly involved in genetic DR-mediated longevity assurance in worms. Identifying these mutation(s) may reveal a novel regulator of longevity required specifically by genetic modes of DR.

scholarly journals The C. elegans Hypertonic Stress Response: Big Insights from Shrinking Worms

2020 ◽  
Vol 55 (S1) ◽  
pp. 89-105
Keyword(s):  
Stress Response ◽  
Cell Volume ◽  
Molecular Mechanisms ◽  
Model Organism ◽  
Future Research ◽  
Transcriptional Level ◽  
Molecular Signaling ◽  
Hypertonic Stress ◽  
Macromolecular Assemblies ◽  
C Elegans

Cell volume is one of the most aggressively defended physiological set points in biology. Changes in intracellular ion and water concentrations, which are induced by changes in metabolism or environmental exposures, disrupt protein folding, enzymatic activity, and macromolecular assemblies. To counter these challenges, cells and organisms have evolved multifaceted, evolutionarily conserved molecular mechanisms to restore cell volume and repair stress induced damage. However, many unanswered questions remain regarding the nature of cell volume 'sensing' as well as the molecular signaling pathways involved in activating physiological response mechanisms. Unbiased genetic screening in the model organism C. elegans is providing new and unexpected insights into these questions, particularly questions relating to the hypertonic stress response (HTSR) pathway. One surprising characteristic of the HTSR pathway in C. elegans is that it is under strong negative regulation by proteins involved in protein homeostasis and the extracellular matrix (ECM). The role of the ECM in particular highlights the importance of studying the HTSR in the context of a live organism where native ECM-tissue associations are preserved. A second novel and recently discovered characteristic is that the HTSR is regulated at the post-transcriptional level. The goal of this review is to describe these discoveries, to provide context for their implications, and to raise outstanding questions to guide future research.

Sign in / Sign up

Export Citation Format

Share Document