Faculty Opinions recommendation of Co-chaperone p23 regulates C. elegans Lifespan in Response to Temperature.

Author(s):  
Seung-Jae V Lee ◽  
Dae-Eun Jeong
2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Wenjing Qi ◽  
Erika D. V. Gromoff ◽  
Fan Xu ◽  
Qian Zhao ◽  
Wei Yang ◽  
...  

AbstractMulticellular organisms coordinate tissue specific responses to environmental information via both cell-autonomous and non-autonomous mechanisms. In addition to secreted ligands, recent reports implicated release of small RNAs in regulating gene expression across tissue boundaries. Here, we show that the conserved poly-U specific endoribonuclease ENDU-2 in C. elegans is secreted from the soma and taken-up by the germline to ensure germline immortality at elevated temperature. ENDU-2 binds to mature mRNAs and negatively regulates mRNA abundance both in the soma and the germline. While ENDU-2 promotes RNA decay in the soma directly via its endoribonuclease activity, ENDU-2 prevents misexpression of soma-specific genes in the germline and preserves germline immortality independent of its RNA-cleavage activity. In summary, our results suggest that the secreted RNase ENDU-2 regulates gene expression across tissue boundaries in response to temperature alterations and contributes to maintenance of stem cell immortality, probably via retaining a stem cell specific program of gene expression.


PLoS Genetics ◽  
2015 ◽  
Vol 11 (4) ◽  
pp. e1005023 ◽  
Author(s):  
Makoto Horikawa ◽  
Surojit Sural ◽  
Ao-Lin Hsu ◽  
Adam Antebi

2020 ◽  
Author(s):  
Zuzana Sekajova ◽  
Elena Rosa ◽  
Foteini Spagopoulou ◽  
Panagiotis-Ioannis Zervakis ◽  
Martin I. Lind

AbstractAnimals are often not growing at the maximum rate, but can compensate for a bad start of life by further increasing growth rate. While this compensatory growth is widespread, its direct fitness consequences are seldom investigated and its genetic basis is unknown. We investigated the genetic regulation, as well as fitness and lifespan consequences of compensatory growth in response to temperature, using C. elegans knockout of the thermo-sensitive TRP ion channel TRPA-1, involved in temperature recognition. We exposed juvenile worms to cold, normal or warm temperatures in order to delay or speed up development. After returning to normal temperature, we found that wild-type worms where early development was delayed, expressed compensatory growth and catched up in size, while juvenile exposure to warm temperatures expressed slowed-down growth and small size. Compensatory growth also altered the reproductive schedule towards early reproduction, so that rate-sensitive individual fitness increased even though total reproduction was unaffected. Surprisingly, no lifespan cost of compensatory growth was found. In contrast, juvenile temperature did not induce compensatory or slowed-down growth in the trpa-1 knockout mutants, and consequently did not affect fitness. We show that temperature-induced compensatory growth in C. elegans is regulated by the trpa-1 and can increase fitness.


2002 ◽  
Vol 69 ◽  
pp. 117-134 ◽  
Author(s):  
Stuart M. Haslam ◽  
David Gems ◽  
Howard R. Morris ◽  
Anne Dell

There is no doubt that the immense amount of information that is being generated by the initial sequencing and secondary interrogation of various genomes will change the face of glycobiological research. However, a major area of concern is that detailed structural knowledge of the ultimate products of genes that are identified as being involved in glycoconjugate biosynthesis is still limited. This is illustrated clearly by the nematode worm Caenorhabditis elegans, which was the first multicellular organism to have its entire genome sequenced. To date, only limited structural data on the glycosylated molecules of this organism have been reported. Our laboratory is addressing this problem by performing detailed MS structural characterization of the N-linked glycans of C. elegans; high-mannose structures dominate, with only minor amounts of complex-type structures. Novel, highly fucosylated truncated structures are also present which are difucosylated on the proximal N-acetylglucosamine of the chitobiose core as well as containing unusual Fucα1–2Gal1–2Man as peripheral structures. The implications of these results in terms of the identification of ligands for genomically predicted lectins and potential glycosyltransferases are discussed in this chapter. Current knowledge on the glycomes of other model organisms such as Dictyostelium discoideum, Saccharomyces cerevisiae and Drosophila melanogaster is also discussed briefly.


2020 ◽  
Vol 48 (3) ◽  
pp. 1019-1034 ◽  
Author(s):  
Rachel M. Woodhouse ◽  
Alyson Ashe

Gene regulatory information can be inherited between generations in a phenomenon termed transgenerational epigenetic inheritance (TEI). While examples of TEI in many animals accumulate, the nematode Caenorhabditis elegans has proven particularly useful in investigating the underlying molecular mechanisms of this phenomenon. In C. elegans and other animals, the modification of histone proteins has emerged as a potential carrier and effector of transgenerational epigenetic information. In this review, we explore the contribution of histone modifications to TEI in C. elegans. We describe the role of repressive histone marks, histone methyltransferases, and associated chromatin factors in heritable gene silencing, and discuss recent developments and unanswered questions in how these factors integrate with other known TEI mechanisms. We also review the transgenerational effects of the manipulation of histone modifications on germline health and longevity.


2020 ◽  
Vol 48 (3) ◽  
pp. 1243-1253 ◽  
Author(s):  
Sukriti Kapoor ◽  
Sachin Kotak

Cellular asymmetries are vital for generating cell fate diversity during development and in stem cells. In the newly fertilized Caenorhabditis elegans embryo, centrosomes are responsible for polarity establishment, i.e. anterior–posterior body axis formation. The signal for polarity originates from the centrosomes and is transmitted to the cell cortex, where it disassembles the actomyosin network. This event leads to symmetry breaking and the establishment of distinct domains of evolutionarily conserved PAR proteins. However, the identity of an essential component that localizes to the centrosomes and promotes symmetry breaking was unknown. Recent work has uncovered that the loss of Aurora A kinase (AIR-1 in C. elegans and hereafter referred to as Aurora A) in the one-cell embryo disrupts stereotypical actomyosin-based cortical flows that occur at the time of polarity establishment. This misregulation of actomyosin flow dynamics results in the occurrence of two polarity axes. Notably, the role of Aurora A in ensuring a single polarity axis is independent of its well-established function in centrosome maturation. The mechanism by which Aurora A directs symmetry breaking is likely through direct regulation of Rho-dependent contractility. In this mini-review, we will discuss the unconventional role of Aurora A kinase in polarity establishment in C. elegans embryos and propose a refined model of centrosome-dependent symmetry breaking.


Author(s):  
Takaaki Hirotsu ◽  
Yu Hayashi ◽  
Ryo Iwata ◽  
Hirofumi Kunitomo ◽  
Eriko Kage-Nakadai ◽  
...  

2010 ◽  
Vol 5 (03) ◽  
Author(s):  
M Pfeiffer ◽  
A Schlotterer ◽  
G Kukudov ◽  
T Fleming ◽  
A Bierhaus ◽  
...  
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