WBbt:0003760 vs long

Reducing the expression of the Indy (Acronym for 'I'm Not Dead, Yet') gene in lower organisms promotes longevity and leads to a phenotype that resembles various aspects of caloric restriction.

With 2,4-dichlorophenol (DCP)-degrading microflora as model microorganisms, this study found that higher dose (10, 100 mg/L) of polystyrene NPs pre-exposure inhibited bacterial DCP degradation prolonging the stagnation period, while lower dose (1 mg/L) of NPs on the contrary stimulated their degradation ability.

In snail control studies using controlled-release formulations only the organotins, especially tributyltin oxide (TBTO), have given satisfactory long-term results.

HAGR features now several databases with high-quality manually curated data: (i) GenAge, a database of genes associated with ageing in humans and model organisms; (ii) AnAge, an extensive collection of longevity records and complementary traits for >4000 vertebrate species; and (iii) GenDR, a newly incorporated database, containing both gene mutations that interfere with dietary restriction-mediated lifespan extension and consistent gene expression changes induced by dietary restriction.

Given that circulating FGF21 can attenuate organelle stress, e.g. mitochondrial and ER stresses, it resembles a stress-induced cell non-autonomous regulation of proteostasis and longevity present in model organisms.

While there are reports on these ERM candidates that describe lifespan extension in model organisms, data on longevity-inducing effects in higher organisms such as mice remain controversial or are missing.

However, systematic studies in single organisms (particularly those that exhibit extreme longevity) are still required to distinguish the fundamental principles concerning the role of methionine and other amino acids in regulating life span.

Exposure to various influences during a critical window of organ growth can interfere with the finely-tuned process of development and induce pathological processes with aberrant alveolarization and long-term structural and functional sequelae.

Several studies across a wide range of model organisms have revealed the involvement of FOXO (forkhead box, class O) transcription factors in orchestrating metabolic homeostasis, as well as in regulating longevity.

Although it is well known that metabolic control plays a crucial role in regulating the health span and life span of various organisms, little is known for the systems metabolic profile of centenarians, the paradigm of human healthy aging and longevity.

Studies in model organisms have identified a variety of genes whose expression can be experimentally modulated to produce changes in longevity, but whether these genes are the same as those involved in natural variation in lifespan remains unclear.

Autophagy increases the lifespan of model organisms; however, its role in promoting mammalian longevity is less well-established1,2.

We investigated the effects of light in the model organism, Drosophila melanogaster, and determined that flies maintained in daily cycles of 12-h blue LED and 12-h darkness had significantly reduced longevity compared with flies maintained in constant darkness or in white light with blue wavelengths blocked.

The budding yeast Saccharomyces cerevisiae has served as a premier model organism for identifying genetic and molecular factors that modulate cellular aging and is a powerful system in which to evaluate candidate longevity interventions.

Insights from organisms, which have evolved natural strategies for promoting survivability under extreme environmental pressures, may help guide future research into novel approaches for enhancing human longevity.

This review examines how organisms regulate nutrient intake and metabolism, focusing on dietary protein's unique role in health and longevity.

Model organisms reveal that longevity and senescence are genetically controlled, but how genes control longevity in different mammalian tissues is unknown.

Using genetically modified model organisms, sirtuins are proved to be one of the most conserved aging-regulatory and longevity-promoting genes/pathways among species.

The findings revealed that, compared to pulmonary, cardiovascular, and metabolic organ damage, 6PPD-Q-induced neurotoxicity was more persistent and irreversible, particularly characterized by prolonged anxiety-like behaviors.

Here, we used the fruit fly (Drosophila melanogaster) as a model organism to determine the epigenetic effects of 0.1% and 1% (w/v) curcumin, which have been shown to promote the health and prolong the lifespan of fruit flies.

In addition to previous results in model organisms like Drosophila melanogaster, recent studies have shown that in mammalian models, aging causes increased intestinal permeability and intestinal-derived systemic inflammation, thereby affecting longevity.

Mutational analyses in model organisms have shown that genes affecting metabolism and stress resistance regulate life span, but the genes responsible for variation in longevity in natural populations are largely unidentified.

Analyses of mutations affecting life span in model organisms have revealed a number of genes that regulate longevity in evolutionarily conserved signaling pathways.

It is proposed that low-intensity stressors, such as CR, activate ancient hormetic defense mechanisms in organisms ranging from yeast to mammals, defending them against a variety of adversities and, when long-term, retarding senescent processes.

Recent findings experimentally link DNA damage and organismal aging: longevity-regulating genetic pathways respond to the accumulation of DNA damage and other stress conditions and conversely influence the rate of damage accumulation and its impact for cancer and aging.

Mechanistically, organismal senescence is caused by a gradual, lifelong accumulation of multifaceted molecular and cellular damage.

When nutrients become sparse as with dietary restriction, growth and development decline, stress response pathways become induced and organisms live longer.

Mucormycosis is a rare, aggressive, and life-threatening infection that is caused by organisms belonging to the order Mucorales.

C. procera caused perforation and tegumental disorganization along with adult worm paralysis.

The present study evaluated interactive effects of metal contamination (cadmium) and pathogenic organisms (trematode parasites Himasthla elongata and pathogenic bacteria Vibrio tapetis) singularly and in combination on the bivalve Ruditapes philippinarum, an introduced species to Europe, under laboratory controlled conditions.

While SC polymerization starts from ZMM-bound sites and ZMM proteins are required for SC polymerization in budding yeast and the fungus Sordaria, other organisms differ in their requirement for ZMM in SC elongation.

The disease is ranked by the World Health Organization (WHO) as the second leading cause of permanent and long-term disability, and has been targeted for elimination by 2020.

Most organisms obtain their fatty acids through their diet or by de novo synthesis, but human blood flukes belonging to the genus Schistosoma lack the oxygen-dependent pathways required for the synthesis of sterols and fatty acids so they are entirely dependent on their hosts for these and other complex lipids.

Compared with other model organisms, Caenorhabditis has several advantages, such as well-defined traits that can be subjected to highly controlled environmental and genetic manipulation and the possibility for long-term experimental evolution that can be coupled with genome-wide mapping of trait variation.

Compared to conventional farming, organic farming increased the population of free-living nematodes and suppressed plant parasitic nematodes belonging to Meloidogynidae and Pratylenchidae.

By this means, autophagy either helps to remove damaged organelles, long-lived proteins and protein aggregates, or serves as a recycling mechanism for molecular building blocks.

In 1995, the disease has been identified by the World Health Organization (WHO) as one of the second leading causes of permanent and long-term disability and thus it is targeted for elimination by year 2020.

In this study, nematodes were used as model organisms that were fed rice kefiran, along with Escherichia coli OP50, as a result of which, the lifespan of nematodes was extended and age-related retardation of mobility was suppressed.

The planar polarized PAR module is then required for actin planar organization, thus contributing to the determination of the orientation of cell-shape changes and the elongation axis of the whole embryo.

However, mechanisms linking their metabolic activities to promote organism longevity remain poorly understood.

Age-induced damage arises due to a decrease in organelle function along with a decline in protein quality control.

Our results demonstrate how inter-organismal signaling during development regulates reproductive maturation and longevity.

Parallel screening employing the simplified model organism Caenorhabditis elegans, fed the Lactobacillus strains as a food source, revealed that one L. pentosus and one L. coryniformis strains significantly induced prolongevity effects and protection from pathogen-mediated infection.

One of the original hypotheses of organismal longevity posits that aging is the natural result of entropy on the cells, tissues, and organs of the animal--a slow, inexorable slide into nonfunctionality caused by stochastic degradation of its parts.

In the majority of the following organisms, muscles formation (steps of determination and the earliest steps of myogenesis) is regulated by genes orthologs Pax3 which belong to the family Pax: nematodes (Caenorhabditis elegans, Pristionchus pacificus), insects (Drosophila melanogaster), echinoderms (Strongylocentrotus purpuratus), sea squirts (Ciona intestinalis, Holocynthia roretzi), fishes (Danio rerio), amphibians (Xenopus laevis), birds, and mammals (mouse, rat).

Pioneering work in model organisms reveals that the reproductive system is involved not only in propagation of the species but also regulates organismal metabolism and longevity.

Thus, in the model organisms C. elegans, resveratrol is capable of promoting longevity at a concentration that pharmacologically relevant and 20 times lower than previously published doses.

Nevertheless, nutritional experiments in model organisms such as yeast, C. elegans, Drosophila, and mice confirm that "caloric restriction" (CR), which is defined generally as a 30-40% decrease in caloric intake, a famine-like condition for humans seen only in the poorest of countries, promotes good health and increases longevity in model organisms.

Other processes that affect organismal longevity, including Jun kinase signaling and caloric restriction, do not affect resistance to bacterial pathogens, further establishing that aging and innate immunity are regulated by genetically distinct mechanisms.

In recent years, genetic intervention of life span regulating pathways, for example, in Drosophila as well as case studies in non-classical animal models, have provided compelling evidence to challenge these views.Rather than comprehensively revisiting studies on the established genetic model systems of ageing, we here focus on an alternative model organism with a wild type (unselected genotype) characterized by a unique diversity in longevity - the honey bee.Honey bee (Apis mellifera) life span varies from a few weeks to more than 2 years.

In these organisms, tumor suppressors such as p53 are central participants in the control of longevity because they regulate stem cell proliferation.

Like other organisms, C. elegans shows both accumulation of habituation with repeated training blocks and long-term retention of spaced or distributed training, but not for massed training.

These mutant animals have defects in the organization of the hypodermal apical actin cytoskeleton that is required for elongation.

The apical organ integrates sensory information and controls the locomotory apparatus of ctenophores, the eight longitudinal rows of ctene/comb plates.

By radiation hybrid mapping, the human gene was localized to a 0.5-centiMorgan region on the long arm of chromosome 1 at q31.3.

In order to elucidate a repertoire of mRNAs regulated by alternative splicing coupled with NMD (AS-NMD) in an organism, we performed long-read RNA sequencing of poly(A)+ RNAs from an NMD-deficient mutant strain of Caenorhabditis elegans, and obtained full-length sequences for mRNA isoforms from 259 high-confidence AS-NMD genes.

Probiotic bacteria, such as lactobacilli, are live microorganisms that exert beneficial effects on human health when ingested in sufficient amounts and can promote longevity.

Caenorhabditis elegans has been used as a major model organism to identify genetic factors that regulate organismal aging and longevity.

Here we show that an organelle network involving lipid droplets and peroxisomes is critical for MUFA-induced longevity in Caenorhabditis elegans.

We previously discovered that four astrocyte-like glia can regulate organismal proteostasis and longevity in C. elegans.

Integrating humanized rodent models, zebrafish, organoids, and induced pluripotent stem cell-based systems-along with advances in bioengineering and genetic editing-may offer a more comprehensive framework to bridge the gap between preclinical research and clinical application.

These studies reveal how metabolic signals and organellar communication regulate a key convergent metabolic transcription factor to promote longevity.

In organisms, long-term nanopolystyrenes (PS-NPs) exposure can cause toxicity, including neurotoxicity.

Finding factors that promote organismal health and longevity therefore holds great therapeutic promise to slow aging and age-associated disease.

The search for probiotic microorganisms that can be applied beyond gut health has advanced into areas that seek to promote longevity and to prevent neurodegenerative diseases.

Moreover, the successful ability of radio waves in biological organisms to produce effects like those produced by blue light, together with their long penetration depth in tissues, stimulates the investigation of radio waves as a substitute for blue light in a non-invasive version of optogenetics.

It has been reported in various model organisms that autophagy and the target of rapamycin complex 1 (TORC1) signaling are strongly involved in eukaryotic cell aging and decreasing TORC1 activity extends longevity by an autophagy-dependent mechanism.

Here we used Drosophila melanogaster as a model organism to examine the role of SIN3 in the regulation of fitness and longevity.

We propose that species with these ancestral gene repertoires are ideal model organisms for studying the genetic regulation of animal longevity and will provide clues to increasing longevity in humans.

C. elegans has been particularly important for exploring the role of innate immunity in organismal stress resistance and the regulation of longevity.

In many organisms, dietary restriction (DR) leads to lifespan extension through the activation of cell protection and pro-longevity gene expression programs.

However, lipidomics, the quantification of all lipid molecules in a biological sample, and genetic studies in model organisms are revealing specific fats that may promote longevity.

Laboratory studies with model organisms may provide additional insight into the long-term effects of altered movement behaviors, such as those caused by human disturbance.

Studies in model organisms suggest that two conserved pathways modulate longevity: DNA damage repair and Insulin/Igf1-like signalling.

Furthermore, this organism may serve as a useful model for gerontologists interested in exploring the mechanisms that promote long life and the slowing of senescence.

Individually, dysfunction of both the endoplasmic reticulum (ER) and mitochondria has been linked to aging, but how communication between these organelles might be targeted to promote longevity is unclear.

In the model organism C. elegans, L-theanine is capable of promoting paraquat resistance and longevity suggesting that this compound may as well promote healthy lifespan in mammals and possibly humans.

These findings support an evolutionarily conserved function for p53 in modulating organismal responses to mitochondrial dysfunction and suggest that metabolic checkpoint responses may play a role in longevity control and in human mitochondrial-associated diseases.