scholarly journals Sex-specific Plasticity and the Nutritional Geometry of Insulin-Signaling Gene Expression in Drosophila Melanogaster

2020 ◽  
Author(s):  
Jeanne M.C. McDonald ◽  
Pegah Nabili ◽  
Lily Thorsen ◽  
Sohee Jeon ◽  
Alexander Shingleton
Keyword(s):  
Body Size ◽  
Protein Level ◽  
Transcriptional Response ◽  
Specific Response ◽  
Dietary Carbohydrate ◽  
Tor Signaling ◽  
Transcriptional Responses ◽  
Low Concentration ◽  
Carbohydrate Level ◽  
Nutritional Geometry

Abstract Background: Sexual-size dimorphism (SSD) is replete among animals, but while the selective pressures that drive the evolution of SSD have been well studied, the developmental mechanisms upon which these pressures act are poorly understood. Ours and others’ research has shown that SSD in Drosophila reflects elevated levels of nutritional plasticity in females versus males, such that SSD increases with dietary intake and body size, a phenomenon called sex-specific plasticity (SSP). Additional data indicate that while body size in both sexes responds to variation in protein level, only female body size is sensitive to variation in carbohydrate level. Here we explore whether these difference in sensitivity at the morphological level are reflected by differences in how the insulin/IGF-signaling (IIS) and TOR-signaling pathways respond to changes in carbohydrates and proteins in females versus males, using a nutritional geometry approach. Results: The IIS-regulated transcripts of 4E-BP and InR most strongly correlated with body size in females and males respectively, but neither responded to carbohydrate level and so could not explain the sex-specific response to body size to dietary carbohydrate. Transcripts regulated by TOR-signaling did, however, respond to dietary carbohydrate in a sex-specific manner. In females, expression of dILP5 positively correlated with body size, while expression of dILP2,3 and 8, was elevated on diets with a low concentration of both carbohydrate and protein. In contrast, we detected lower levels of dILP2 and 5 protein in the brains of females fed on low concentration diets. We could not detect any effect of diet on dILP expression in males.Conclusion: Although females and males show sex-specific transcriptional responses to changes in protein and carbohydrate, the patterns of expression do not support a simple model of the regulation of body-size SSP by either insulin- or TOR-signaling. The data also indicate a complex relationship between carbohydrate and protein level, dILP expression and dILP peptide levels in the brain. In general, diet quality and sex both affect the transcriptional response to changes in diet quantity, and so should be considered in future studies that explore the effect of nutrition on body size.

scholarly journals Sex-specific plasticity and the nutritional geometry of insulin-signaling gene expression in Drosophila melanogaster

EvoDevo ◽  
2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Jeanne M. C. McDonald ◽  
Pegah Nabili ◽  
Lily Thorsen ◽  
Sohee Jeon ◽  
Alexander W. Shingleton
Keyword(s):  
Body Size ◽  
Protein Level ◽  
Transcriptional Response ◽  
Specific Response ◽  
Dietary Carbohydrate ◽  
Tor Signaling ◽  
Transcriptional Responses ◽  
Low Concentration ◽  
Carbohydrate Level ◽  
Nutritional Geometry

Abstract Background Sexual-size dimorphism (SSD) is replete among animals, but while the selective pressures that drive the evolution of SSD have been well studied, the developmental mechanisms upon which these pressures act are poorly understood. Ours and others’ research has shown that SSD in D. melanogaster reflects elevated levels of nutritional plasticity in females versus males, such that SSD increases with dietary intake and body size, a phenomenon called sex-specific plasticity (SSP). Additional data indicate that while body size in both sexes responds to variation in protein level, only female body size is sensitive to variation in carbohydrate level. Here, we explore whether these difference in sensitivity at the morphological level are reflected by differences in how the insulin/IGF-signaling (IIS) and TOR-signaling pathways respond to changes in carbohydrates and proteins in females versus males, using a nutritional geometry approach. Results The IIS-regulated transcripts of 4E-BP and InR most strongly correlated with body size in females and males, respectively, but neither responded to carbohydrate level and so could not explain the sex-specific response to body size to dietary carbohydrate. Transcripts regulated by TOR-signaling did, however, respond to dietary carbohydrate in a sex-specific manner. In females, expression of dILP5 positively correlated with body size, while expression of dILP2,3 and 8, was elevated on diets with a low concentration of both carbohydrate and protein. In contrast, we detected lower levels of dILP2 and 5 protein in the brains of females fed on low concentration diets. We could not detect any effect of diet on dILP expression in males. Conclusion Although females and males show sex-specific transcriptional responses to changes in protein and carbohydrate, the patterns of expression do not support a simple model of the regulation of body-size SSP by either insulin- or TOR-signaling. The data also indicate a complex relationship between carbohydrate and protein level, dILP expression and dILP peptide levels in the brain. In general, diet quality and sex both affect the transcriptional response to changes in diet quantity, and so should be considered in future studies that explore the effect of nutrition on body size.

scholarly journals Sex-specific plasticity and the nutritional geometry of insulin-signaling gene expression in Drosophila melanogaster

2020 ◽  
Author(s):  
Jeanne M.C. McDonald ◽  
Pegah Nabili ◽  
Lily Thorsen ◽  
Sohee Jeon ◽  
Alexander Shingleton
Keyword(s):  
Body Size ◽  
Protein Level ◽  
Transcriptional Response ◽  
Specific Response ◽  
Dietary Carbohydrate ◽  
Tor Signaling ◽  
Transcriptional Responses ◽  
Low Concentration ◽  
Carbohydrate Level ◽  
Nutritional Geometry

1.AbstractBackgroundSexual-size dimorphism (SSD) is replete among animals, but while the selective pressures that drive the evolution of SSD have been well studied, the developmental mechanisms upon which these pressures act are poorly understood. Ours and others’ research has shown that SSD in Drosophila reflects elevated levels of nutritional plasticity in females versus males, such that SSD increases with dietary intake and body size, a phenomenon called sex-specific plasticity (SSP). Additional data indicate that while body size in both sexes responds to variation in protein level, only female body size is sensitive to variation in carbohydrate level. Here we explore whether these difference in sensitivity at the morphological level are reflected by differences in how the insulin/IGF-signaling (IIS) and TOR-signaling pathways respond to changes in carbohydrates and proteins in females versus males, using a nutritional geometry approach.ResultsThe IIS-regulated transcripts of 4E-BP and InR most strongly correlated with body size in females and males respectively, but neither responded to carbohydrate level and so could not explain the sex-specific response to body size to dietary carbohydrate. Transcripts regulated by TOR-signaling did, however, respond to dietary carbohydrate in a sex-specific manner. In females, expression of dILP5 positively correlated with body size, while expression of dILP2,3 and 8, was elevated on diets with a low concentration of both carbohydrate and protein. In contrast, we detected lower levels of dILP2 and 5 protein in the brains of females fed on low concentration diets. We could not detect any effect of diet on dILP expression in males.ConclusionAlthough females and males show sex-specific transcriptional responses to changes in protein and carbohydrate, the patterns of expression do not support a simple model of the regulation of body-size SSP by either insulin-or TOR-signaling. The data also indicate a complex relationship between carbohydrate and protein level, dILP expression and dILP peptide levels in the brain. In general, diet quality and sex both affect the transcriptional response to changes in diet quantity, and so should be considered in future studies that explore the effect of nutrition on body size.

scholarly journals Mycobacterium tuberculosis canonical virulence factors interfere with a late component of the TLR2 response.

2021 ◽  
Author(s):  
Amelia E. Hinman ◽  
Charul Jani ◽  
Stephanie C. Pringle ◽  
Wei R. Zhang ◽  
Neharika Jain ◽  
...  
Keyword(s):  
Mycobacterium Tuberculosis ◽  
Virulence Factors ◽  
Pathogenic Bacteria ◽  
Membrane Damage ◽  
Transcriptional Response ◽  
Specific Response ◽  
Late Component ◽  
Transcriptional Responses ◽  
Phagosomal Membrane ◽  
Endosomal Uptake

For many intracellular pathogens, the phagosome is the site of events and interactions that shape infection outcome. Phagosomal membrane damage, in particular, is proposed to benefit invading pathogens. To define the innate immune consequences of this damage, we profiled macrophage transcriptional responses to wild-type Mycobacterium tuberculosis (Mtb) and mutants that fail to damage the phagosomal membrane. We identified a set of genes with enhanced expression in response to the mutants. These genes represented a late component of the TLR2-dependent transcriptional response to Mtb, distinct from an earlier component that included TNF. Expression of the later component was inherent to TLR2 activation, dependent upon endosomal uptake, and enhanced by phagosome acidification. Canonical Mtb virulence factors that contribute to phagosomal membrane damage blunted phagosome acidification and undermined the endosome-specific response. Profiling cell survival and bacterial growth in macrophages demonstrated that the attenuation of these mutants is partially dependent upon TLR2. Further, TLR2 contributed to the attenuated phenotype of one of these mutants in a murine model of infection. These results demonstrate two distinct components of the TLR2 response and identify a component dependent upon endosomal uptake as a point where pathogenic bacteria interfere with the generation of effective inflammation. This interference promotes TB pathogenesis in both macrophage and murine infection models.

scholarly journals Mycobacterium tuberculosis canonical virulence factors interfere with a late component of the TLR2 response

eLife ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
Amelia E Hinman ◽  
Charul Jani ◽  
Stephanie C Pringle ◽  
Wei R Zhang ◽  
Neharika Jain ◽  
...  
Keyword(s):  
Mycobacterium Tuberculosis ◽  
Virulence Factors ◽  
Pathogenic Bacteria ◽  
Membrane Damage ◽  
Transcriptional Response ◽  
Specific Response ◽  
Late Component ◽  
Transcriptional Responses ◽  
Phagosomal Membrane ◽  
Endosomal Uptake

For many intracellular pathogens, the phagosome is the site of events and interactions that shape infection outcome. Phagosomal membrane damage, in particular, is proposed to benefit invading pathogens. To define the innate immune consequences of this damage, we profiled macrophage transcriptional responses to wild-type Mycobacterium tuberculosis (Mtb) and mutants that fail to damage the phagosomal membrane. We identified a set of genes with enhanced expression in response to the mutants. These genes represented a late component of the TLR2-dependent transcriptional response to Mtb, distinct from an earlier component that included Tnf. Expression of the later component was inherent to TLR2 activation, dependent upon endosomal uptake, and enhanced by phagosome acidification. Canonical Mtb virulence factors that contribute to phagosomal membrane damage blunted phagosome acidification and undermined the endosome-specific response. Profiling cell survival and bacterial growth in macrophages demonstrated that the attenuation of these mutants is partially dependent upon TLR2. Further, TLR2 contributed to the attenuated phenotype of one of these mutants in a murine model of infection. These results demonstrate two distinct components of the TLR2 response and identify a component dependent upon endosomal uptake as a point where pathogenic bacteria interfere with the generation of effective inflammation. This interference promotes TB pathogenesis in both macrophage and murine infection models.

scholarly journals Tumor hypoxia induces nuclear paraspeckle formation through HIF-2α dependent transcriptional activation of NEAT1 leading to cancer cell survival

Oncogene ◽  
2014 ◽  
Vol 34 (34) ◽  
pp. 4482-4490 ◽  
Author(s):  
H Choudhry ◽  
A Albukhari ◽  
M Morotti ◽  
S Haider ◽  
D Moralli ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cell ◽  
Transcriptional Activation ◽  
Cellular Proliferation ◽  
Hypoxia Inducible Factor ◽  
Tumor Hypoxia ◽  
Transcriptional Response ◽  
Clonogenic Survival ◽  
Breast Cancer Cell Lines ◽  
Transcriptional Responses

Abstract Activation of cellular transcriptional responses, mediated by hypoxia-inducible factor (HIF), is common in many types of cancer, and generally confers a poor prognosis. Known to induce many hundreds of protein-coding genes, HIF has also recently been shown to be a key regulator of the non-coding transcriptional response. Here, we show that NEAT1 long non-coding RNA (lncRNA) is a direct transcriptional target of HIF in many breast cancer cell lines and in solid tumors. Unlike previously described lncRNAs, NEAT1 is regulated principally by HIF-2 rather than by HIF-1. NEAT1 is a nuclear lncRNA that is an essential structural component of paraspeckles and the hypoxic induction of NEAT1 induces paraspeckle formation in a manner that is dependent upon both NEAT1 and on HIF-2. Paraspeckles are multifunction nuclear structures that sequester transcriptionally active proteins as well as RNA transcripts that have been subjected to adenosine-to-inosine (A-to-I) editing. We show that the nuclear retention of one such transcript, F11R (also known as junctional adhesion molecule 1, JAM1), in hypoxia is dependent upon the hypoxic increase in NEAT1, thereby conferring a novel mechanism of HIF-dependent gene regulation. Induction of NEAT1 in hypoxia also leads to accelerated cellular proliferation, improved clonogenic survival and reduced apoptosis, all of which are hallmarks of increased tumorigenesis. Furthermore, in patients with breast cancer, high tumor NEAT1 expression correlates with poor survival. Taken together, these results indicate a new role for HIF transcriptional pathways in the regulation of nuclear structure and that this contributes to the pro-tumorigenic hypoxia-phenotype in breast cancer.

scholarly journals Penentuan Kadar Protein dan Karbohidrat pada Limbah Batang Pohon Pisang Kepok (Musa paradisiaca normalis)

2018 ◽  
Vol 7 (4) ◽  
pp. 168
Author(s):  
Noviasri Dhamayanti ◽  
Vanny M. A. Tiwow ◽  
Siti Nuryanti
Keyword(s):  
Protein Level ◽  
Reducing Sugar ◽  
Soft Layer ◽  
Hard Layer ◽  
Musa Paradisiaca ◽  
Banana Tree ◽  
Carbohydrate Level ◽  
Kjeldahl Method ◽  
Carbohydrate Levels ◽  
Central Sulawesi

The aim of this study was to determine protein and carbohydrate levels contained in waste of banana kepok (Musa paradisiaca Normalis) trees. Samples were taken from Mpanau Sigi Central Sulawesi. This study used Kjeldahl method in determining protein level, and anthrone method in determining reducing sugar level. The analysis results obtained in the hard layer of banana tree are 3.05% of protein level and 6.75% of carbohydrate level, while in the soft layer of banana tree are 0.08% of protein level and 4.75% of carbohydrate level, respectively. This study concluded that protein and carbohydrate levels obtained from the hard layer of banana kepok trees waste is higher, than literatures.

scholarly journals The dynamic effect of regulatory genetic variation on the in vivo ER stress transcriptional response

2021 ◽  
Author(s):  
Nikki D. Russell ◽  
Clement Y. Chow
Keyword(s):  
Genetic Variation ◽  
Stress Response ◽  
Er Stress ◽  
Transcriptional Response ◽  
Mouse Strains ◽  
Transcriptional Responses ◽  
Er Stress Response ◽  
Multiple Environments ◽  
Context Specific

AbstractGenotype x Environment (GxE) interactions occur when environmental conditions drastically change the effect of a genetic variant. In order to truly understand the effect of genetic variation, we need to incorporate multiple environments into our analyses. Many variants, under steady state conditions, may be silent or even have the opposite effect under stress conditions. This study uses an in vivo mouse model to investigate how the effect of genetic variation changes with tissue type and cellular stress. Endoplasmic reticulum (ER) stress occurs when misfolded proteins accumulate in the ER. This triggers the unfolded protein response (UPR), a large transcriptional response which attempts to return the cell to homeostasis. This transcriptional response, despite being a well conserved, basic cellular process, is highly variable across different genetic backgrounds, making it an ideal system to study GxE effects. In this study, we sought to better understand how genetic variation alters expression across tissues, in the presence and absence of ER stress. The use of different mouse strains and their F1s allow us to also identify context specific cis- and trans-regulatory mechanisms underlying variable transcriptional responses. We found hundreds of genes that respond to ER stress in a tissue- and/or genotype-dependent manner. Genotype-dependent ER stress-responsive genes are enriched for processes such as protein folding, apoptosis, and protein transport, indicating that some of the variability occurs in canonical ER stress factors. The majority of regulatory mechanisms underlying these variable transcriptional responses derive from cis-regulatory variation and are unique to a given tissue or ER stress state. This study demonstrates the need for incorporating multiple environments in future studies to better elucidate the effect of any particular genetic factor in basic biological pathways, like the ER stress response.Author SummaryThe effect of genetic variation is dependent on environmental context. Here we use genetically diverse mouse strains to understand how genetic variation interacts with stress state to produce variable transcriptional profiles. In this study, we take advantage of the endoplasmic reticulum (ER) stress response which is a large transcriptional response to misfolded proteins. Using this system, we uncovered tissue- and ER stress-specific effects of genetic variation on gene expression. Genes with genotype-dependent variable expression levels in response to ER stress were enriched for canonical ER stress functions, such as protein folding and transport. These variable effects of genetic variation are driven by unique sets of regulatory variation that are only active under context-specific circumstances. The results of this study highlight the importance of including multiple environments and genetic backgrounds when studying the ER stress response and other cellular pathways.

scholarly journals Hap2-3-5-Gln3 determine transcriptional activation of GDH1 and ASN1 under repressive nitrogen conditions in the yeast Saccharomyces cerevisiae

Microbiology ◽  
2011 ◽  
Vol 157 (3) ◽  
pp. 879-889 ◽  
Author(s):  
Hugo Hernández ◽  
Cristina Aranda ◽  
Geovani López ◽  
Lina Riego ◽  
Alicia González
Keyword(s):  
Dna Binding ◽  
Transcriptional Activation ◽  
Specific Binding ◽  
Transcriptional Response ◽  
Transcriptional Regulator ◽  
Transcriptional Responses ◽  
Yeast Saccharomyces Cerevisiae ◽  
Activation Domains ◽  
Transcriptional Complex ◽  
Nitrogen Conditions

The transcriptional activation response relies on a repertoire of transcriptional activators, which decipher regulatory information through their specific binding to cognate sequences, and their capacity to selectively recruit the components that constitute a given transcriptional complex. We have addressed the possibility of achieving novel transcriptional responses by the construction of a new transcriptional regulator – the Hap2-3-5-Gln3 hybrid modulator – harbouring the HAP complex polypeptides that constitute the DNA-binding domain (Hap2-3-5) and the Gln3 activation domain, which usually act in an uncombined fashion. The results presented in this paper show that transcriptional activation of GDH1 and ASN1 under repressive nitrogen conditions is achieved through the action of the novel Hap2-3-5-Gln3 transcriptional regulator. We propose that the combination of the Hap DNA-binding and Gln3 activation domains results in a hybrid modulator that elicits a novel transcriptional response not evoked when these modulators act independently.

scholarly journals Transcriptional Profiling of Colicin-Induced Cell Death of Escherichia coli MG1655 Identifies Potential Mechanisms by Which Bacteriocins Promote Bacterial Diversity

2004 ◽  
Vol 186 (3) ◽  
pp. 866-869 ◽  
Author(s):  
Daniel Walker ◽  
Matthew Rolfe ◽  
Arthur Thompson ◽  
Geoffrey R. Moore ◽  
Richard James ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Transcriptional Profiling ◽  
Transcriptional Response ◽  
Chromosomal Dna ◽  
Transcriptional Responses ◽  
General Role ◽  
Bacterial Physiology ◽  
Translational Arrest ◽  
Colicin E3 ◽  
Colicin E9

ABSTRACT We report the transcriptional response of Escherichia coli MG1655 to damage induced by colicins E3 and E9, bacteriocins that kill cells through inactivation of the ribosome and degradation of chromosomal DNA, respectively. Colicin E9 strongly induced the LexA-regulated SOS response, while colicin E3 elicited a broad response that included the induction of cold shock genes, symptomatic of translational arrest. Colicin E3 also increased the transcription of cryptic prophage genes and other laterally acquired mobile elements. The transcriptional responses to both these toxins suggest mechanisms that may promote genetic diversity in E. coli populations, pointing to a more general role for colicins in adaptive bacterial physiology than has hitherto been realized.

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