Caenorhabditis elegans unc-37/groucho Interacts Genetically With Components of the Transcriptional Mediator Complex

Genetics ◽  
2002 ◽  
Vol 160 (2) ◽  
pp. 799-803
Author(s):  
Hong Zhang ◽  
Scott W Emmons
Keyword(s):  
Caenorhabditis Elegans ◽  
Sensory Neurons ◽  
Chromatin Structure ◽  
Synthetic Lethality ◽  
Mediator Complex ◽  
Developmental Processes ◽  
Basal Transcriptional Machinery ◽  
Transcriptional Machinery

Abstract Groucho functions as a general corepressor by modulating chromatin structure and has a widespread role in many developmental processes. Here we show that Groucho may also interact with the basal transcriptional machinery. Mutations in Caenorhabditis elegans groucho interact with mutations in components of the transcriptional Mediator complex, resulting in synthetic lethality and loss of male sensory neurons.

scholarly journals Steroid hormones sulfatase inactivation extends lifespan and ameliorates age-related diseases

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Mercedes M. Pérez-Jiménez ◽  
José M. Monje-Moreno ◽  
Ana María Brokate-Llanos ◽  
Mónica Venegas-Calerón ◽  
Alicia Sánchez-García ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Caenorhabditis Elegans ◽  
Protein Aggregation ◽  
Steroid Hormones ◽  
Sensory Neurons ◽  
Environmental Cues ◽  
Steroid Sulfatase ◽  
Loss Of Function ◽  
C Elegans ◽  
Age Related

AbstractAging and fertility are two interconnected processes. From invertebrates to mammals, absence of the germline increases longevity. Here we show that loss of function of sul-2, the Caenorhabditis elegans steroid sulfatase (STS), raises the pool of sulfated steroid hormones, increases longevity and ameliorates protein aggregation diseases. This increased longevity requires factors involved in germline-mediated longevity (daf-16, daf-12, kri-1, tcer-1 and daf-36 genes) although sul-2 mutations do not affect fertility. Interestingly, sul-2 is only expressed in sensory neurons, suggesting a regulation of sulfated hormones state by environmental cues. Treatment with the specific STS inhibitor STX64, as well as with testosterone-derived sulfated hormones reproduces the longevity phenotype of sul-2 mutants. Remarkably, those treatments ameliorate protein aggregation diseases in C. elegans, and STX64 also Alzheimer’s disease in a mammalian model. These results open the possibility of reallocating steroid sulfatase inhibitors or derivates for the treatment of aging and aging related diseases.

scholarly journals Circuit mechanisms encoding odors and driving aging-associated behavioral declines in Caenorhabditis elegans

eLife ◽  
2015 ◽  
Vol 4 ◽  
Author(s):  
Sarah G Leinwand ◽  
Claire J Yang ◽  
Daphne Bazopoulou ◽  
Nikos Chronis ◽  
Jagan Srinivasan ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Sensory Neurons ◽  
Neural Activity ◽  
Chemical Cues ◽  
Primary Neurons ◽  
Olfactory Neurons ◽  
Odor Concentration ◽  
Evoked Activity ◽  
Sensory Neural ◽  
Extract Information

Chemosensory neurons extract information about chemical cues from the environment. How is the activity in these sensory neurons transformed into behavior? Using Caenorhabditis elegans, we map a novel sensory neuron circuit motif that encodes odor concentration. Primary neurons, AWCON and AWA, directly detect the food odor benzaldehyde (BZ) and release insulin-like peptides and acetylcholine, respectively, which are required for odor-evoked responses in secondary neurons, ASEL and AWB. Consistently, both primary and secondary neurons are required for BZ attraction. Unexpectedly, this combinatorial code is altered in aged animals: odor-evoked activity in secondary, but not primary, olfactory neurons is reduced. Moreover, experimental manipulations increasing neurotransmission from primary neurons rescues aging-associated neuronal deficits. Finally, we correlate the odor responsiveness of aged animals with their lifespan. Together, these results show how odors are encoded by primary and secondary neurons and suggest reduced neurotransmission as a novel mechanism driving aging-associated sensory neural activity and behavioral declines.

scholarly journals The AFD Sensory Neurons Encode Multiple Functions Underlying Thermotactic Behavior in Caenorhabditis elegans

2006 ◽  
Vol 26 (28) ◽  
pp. 7444-7451 ◽  
Author(s):  
D. A. Clark ◽  
D. Biron ◽  
P. Sengupta ◽  
A. D. T. Samuel
Keyword(s):  
Caenorhabditis Elegans ◽  
Sensory Neurons ◽  
Multiple Functions

scholarly journals Expression of an expanded CGG-repeat RNA in a single pair of primary sensory neurons impairs olfactory adaptation in Caenorhabditis elegans

2014 ◽  
Vol 23 (18) ◽  
pp. 4945-4959 ◽  
Author(s):  
Bi-Tzen Juang ◽  
Anna L. Ludwig ◽  
Kelli L. Benedetti ◽  
Chen Gu ◽  
Kimberly Collins ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Sensory Neurons ◽  
Single Pair ◽  
Primary Sensory Neurons ◽  
Cgg Repeat ◽  
Olfactory Adaptation

Ultrasound neuro-modulation chip: activation of sensory neurons in Caenorhabditis elegans by surface acoustic waves

Lab on a Chip ◽  
2017 ◽  
Vol 17 (10) ◽  
pp. 1725-1731 ◽  
Author(s):  
Wei Zhou ◽  
Jingjing Wang ◽  
Kaiyue Wang ◽  
Bin Huang ◽  
Lili Niu ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Sensory Neurons ◽  
Acoustic Waves ◽  
Surface Acoustic Waves ◽  
C Elegans

We demonstrate an ultrasound neuro-modulation chip capable of activating neurons of the C. elegans directly.

Effects of genetic variation on chromatin structure and the transcriptional machinery: analysis of the IL6 gene locus

2012 ◽  
Vol 13 (7) ◽  
pp. 583-586 ◽  
Author(s):  
A J P Smith ◽  
D Zheng ◽  
J Palmen ◽  
D X Pang ◽  
P Woo ◽  
...  
Keyword(s):  
Genetic Variation ◽  
Chromatin Structure ◽  
Gene Locus ◽  
Transcriptional Machinery ◽  
Il6 Gene

scholarly journals Feeding state-dependent regulation of developmental plasticity via CaMKI and neuroendocrine signaling

eLife ◽  
2015 ◽  
Vol 4 ◽  
Author(s):  
Scott J Neal ◽  
Asuka Takeishi ◽  
Michael P O'Donnell ◽  
JiSoo Park ◽  
Myeongjin Hong ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Subcellular Localization ◽  
Sensory Neurons ◽  
Reproductive Cycle ◽  
Neuronal Network ◽  
Nutrient Availability ◽  
Developmental Plasticity ◽  
State Dependent ◽  
Dauer Formation ◽  
Growth Promoting

Information about nutrient availability is assessed via largely unknown mechanisms to drive developmental decisions, including the choice of Caenorhabditis elegans larvae to enter into the reproductive cycle or the dauer stage. In this study, we show that CMK-1 CaMKI regulates the dauer decision as a function of feeding state. CMK-1 acts cell-autonomously in the ASI, and non cell-autonomously in the AWC, sensory neurons to regulate expression of the growth promoting daf-7 TGF-β and daf-28 insulin-like peptide (ILP) genes, respectively. Feeding state regulates dynamic subcellular localization of CMK-1, and CMK-1-dependent expression of anti-dauer ILP genes, in AWC. A food-regulated balance between anti-dauer ILP signals from AWC and pro-dauer signals regulates neuroendocrine signaling and dauer entry; disruption of this balance in cmk-1 mutants drives inappropriate dauer formation under well-fed conditions. These results identify mechanisms by which nutrient information is integrated in a small neuronal network to modulate neuroendocrine signaling and developmental plasticity.

scholarly journals Antagonistic regulation of trafficking to Caenorhabditis elegans sensory cilia by a Retinal Degeneration 3 homolog and retromer

2017 ◽  
Vol 115 (3) ◽  
pp. E438-E447 ◽  
Author(s):  
Luis A. Martínez-Velázquez ◽  
Niels Ringstad
Keyword(s):  
Caenorhabditis Elegans ◽  
Retinal Degeneration ◽  
Sensory Neurons ◽  
Secretory Pathway ◽  
Early Stage ◽  
Sensory Modality ◽  
Retinal Dystrophy ◽  
Sensory Transduction ◽  
Sensory Receptor

Sensory neurons often possess cilia with elaborate membrane structures that are adapted to the sensory modality of the host cell. Mechanisms that target sensory transduction proteins to these specialized membrane domains remain poorly understood. Here, we show that a homolog of the human retinal dystrophy gene Retinal Degeneration 3 (RD3) is a Golgi-associated protein required for efficient trafficking of a sensory receptor, the receptor-type guanylate cyclase GCY-9, to cilia in chemosensory neurons of the nematode Caenorhabditis elegans. The trafficking defect caused by mutation of the nematode RD3 homolog is suppressed in vivo by mutation of key components of the retromer complex, which mediates recycling of cargo from endosomes to the Golgi. Our data show that there exists a critical balance in sensory neurons between the rates of anterograde and retrograde trafficking of cargo destined for the sensory cilium and this balance requires molecular specialization at an early stage of the secretory pathway.

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