scholarly journals Serotonin signaling by maternal neurons upon stress ensures progeny survival

eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
Srijit Das ◽  
Felicia K Ooi ◽  
Johnny Cruz Corchado ◽  
Leah C Fuller ◽  
Joshua A Weiner ◽  
...  
Keyword(s):  
Germ Cells ◽  
Mammalian Cells ◽  
Response Times ◽  
Signal Transduction Pathway ◽  
Serotonin Release ◽  
Transduction Pathway ◽  
C Elegans ◽  
Serotonin Signaling ◽  
Stress Sensing ◽  
Protective Gene

Germ cells are vulnerable to stress. Therefore, how organisms protect their future progeny from damage in a fluctuating environment is a fundamental question in biology. We show that in Caenorhabditis elegans, serotonin released by maternal neurons during stress ensures the viability and stress resilience of future offspring. Serotonin acts through a signal transduction pathway conserved between C. elegans and mammalian cells to enable the transcription factor HSF1 to alter chromatin in soon-to-be fertilized germ cells by recruiting the histone chaperone FACT, displacing histones, and initiating protective gene expression. Without serotonin release by maternal neurons, FACT is not recruited by HSF1 in germ cells, transcription occurs but is delayed, and progeny of stressed C. elegans mothers fail to complete development. These studies uncover a novel mechanism by which stress sensing by neurons is coupled to transcription response times of germ cells to protect future offspring.

scholarly journals Serotonin signaling by maternal neurons upon stress ensures progeny survival

2020 ◽  
Author(s):  
Srijit Das ◽  
Felicia K. Ooi ◽  
Johnny Cruz Corchado ◽  
Leah C. Fuller ◽  
Joshua A. Weiner ◽  
...  
Keyword(s):  
Germ Cells ◽  
Mammalian Cells ◽  
Response Times ◽  
Signal Transduction Pathway ◽  
Transduction Pathway ◽  
C Elegans ◽  
Complete Development ◽  
Serotonin Signaling ◽  
Stress Sensing ◽  
Protective Gene

AbstractGerm cells are vulnerable to stress. Therefore, how organisms protect their future progeny from damage in a fluctuating environment is a fundamental question in biology. We show that in Caenorhabditis elegans, serotonin released by maternal neurons during stress ensures the viability and stress tolerance of future offspring by enabling the transcription factor HSF1 to alter chromatin in soon-to-be fertilized germ cells by recruiting the histone chaperone FACT, displacing histones, and initiating protective gene expression. Without maternal serotonin signaling by neurons, FACT is not recruited by HSF1 in germ cells, transcription occurs but is delayed, and progeny of stressed C. elegans mothers fail to complete development. Serotonin acts through a signal transduction pathway conserved between C. elegans and mammalian cells to facilitate HSF1 to recruit FACT. These studies uncover a novel mechanism by which stress sensing by neurons is coupled to transcription response times of germ cells to protect future offspring.

Genetic regulation of entry into meiosis in Caenorhabditis elegans

Development ◽  
1998 ◽  
Vol 125 (10) ◽  
pp. 1803-1813 ◽  
Author(s):  
L.C. Kadyk ◽  
J. Kimble
Keyword(s):  
Signal Transduction ◽  
Caenorhabditis Elegans ◽  
Germ Cells ◽  
Genetic Regulation ◽  
Signal Transduction Pathway ◽  
Mitotic Cell ◽  
Transduction Pathway ◽  
Germline Development ◽  
Large Tumor ◽  
Regulatory Pathways

The Caenorhabditis elegans germline is composed of mitotically dividing cells at the distal end that give rise to meiotic cells more proximally. Specification of the distal region as mitotic relies on induction by the somatic distal tip cell and the glp-1 signal transduction pathway. However, the genetic control over the transition from mitosis to meiosis is not understood. In this paper, we report the identification of a gene, gld-2, that has at least two functions in germline development. First, gld-2 is required for normal progression through meiotic prophase. Second, gld-2 promotes entry into meiosis from the mitotic cell cycle. With respect to this second function, gld-2 appears to be functionally redundant with a previously described gene, gld-1 (Francis, R., Barton, M. K., Kimble, J. and Schedl, T. (1995) Genetics 139, 579–606). Germ cells in gld-1(o) and gld-2 single mutants enter meiosis at the normal time, but germ cells in gld-2 gld-1(o) double mutants do not enter meiosis. Instead, the double mutant germline is mitotic throughout and forms a large tumor. We suggest that gld-1 and gld-2 define two independent regulatory pathways, each of which can be sufficient for entry into meiosis. Epistasis analyses show that gld-1 and gld-2 work downstream of the glp-1 signal transduction pathway. Therefore, we hypothesize that glp-1 promotes proliferation by inhibiting the meiosis-promoting functions of gld-1 and gld-2.

CK2 Is Acting Upstream of MEK3/6 as a Part of the Signal Control of ERK1/2 and p38 MAPK during Keratinocytes Autocrine Differentiation

2011 ◽  
Vol 66 (1-2) ◽  
pp. 83-86 ◽  
Author(s):  
Antonia R. Isaeva ◽  
Vanio I. Mitev
Keyword(s):  
Signal Transduction ◽  
P38 Mapk ◽  
Mammalian Cells ◽  
Protein Kinase Ck2 ◽  
Cell Signalling ◽  
Signal Transduction Pathway ◽  
Signal Control ◽  
Transduction Pathway ◽  
Protein Levels ◽  
Kinase Ck2

Protein kinase CK2 (formerly termed “casein kinase II”) is a ubiquitously in mammalian cells distributed Ser/Thr kinase, with global role in cell regulation. Although, the involvement of CK2 in cell signalling is vast-investigated, virtually nothing is known about its contribution to signal control of keratinocytes differentiation. Here we show that, in autocrine differentiating keratinocytes, inhibition of the CK2 activity induced by 4,5,6,7-tetrabromobenzotriazole (TBB) causes reciprocal changes in the activities of major signal transduction regulators of keratinocytes differentiation, i.e. ERK1/2 and p38 MAPK, without affecting their protein levels. The ERK1/2 activity is strongly suppressed, while the activity of p38 is increased. We have also found that the activity of upstream and specifi c for p38 MAPK kinase MEK3/6 is also stimulated by TBB. These original results clearly demonstrate the participation of CK2 in the signal transduction pathway controlling MEK3/6, p38 MAPK, and ERK1/2 in the used model system.

An osmosensing signal transduction pathway in mammalian cells

Science ◽  
1994 ◽  
Vol 265 (5173) ◽  
pp. 806-808 ◽  
Author(s):  
Z Galcheva-Gargova ◽  
B Derijard ◽  
I. Wu ◽  
R. Davis
Keyword(s):  
Signal Transduction ◽  
Mammalian Cells ◽  
Signal Transduction Pathway ◽  
Transduction Pathway

scholarly journals Inhibition of ULK2 Autophagic Activity by Its Association with YAP

2016 ◽  
Vol 8 (1) ◽  
pp. 12 ◽  
Author(s):  
Sung Hwa Shin ◽  
Eun Jeoung Lee ◽  
Sunghee Hyun ◽  
Dowonkyoung Park ◽  
Sang Sun Kang
Keyword(s):  
Mammalian Cells ◽  
Signal Transduction Pathway ◽  
Transduction Pathway ◽  
Wild Type ◽  
Therapeutic Approaches ◽  
Serine Threonine Kinase ◽  
Threonine Kinase ◽  
Py Motif

Uncoordinated 51-like kinase 2 (ULK2) is a member of the serine/threonine kinase family that functions an essential role regulating autophagy in mammalian cells. As autophagy is implicated in normal cellular homeostasis and multiple diseases, better mechanisticinsight will drive thedevelopment of novel therapeutic approaches. Here, we present evidence that ULK2 interacts withYAP for its degradation and subcellular localization. A potential PPxY motif (328PPnY331) was identified, which is similar with the consensus PPxY motif in ULK2 S/P domain. TheP329A (PA) mutation in the PY motif of ULK2 abolished the YAP-ULK2 association.At first, we observed that ULK2 physically interacted to YAP in vivo and in vitro, using a pull-down approach. Secondly, ULK2 and YAP co- localized at the apical (or tight junction) membrane as visualized by confocal microscopy. Furthermore, the PA mutant substantially increased during autophagy than that of wild-type ULK2 or the P242A mutant in transient transfection assays. Thus, the association between ULK2 and YAP through the WW domain links autophagy and the Hippo signal transduction pathway.

scholarly journals Signalling of abscisic acid to regulate plant growth

1998 ◽  
Vol 353 (1374) ◽  
pp. 1439-1444 ◽  
Author(s):  
Axel Himmelbach ◽  
Monika Iten ◽  
Erwin Grill
Keyword(s):  
Signal Transduction ◽  
Abscisic Acid ◽  
Mammalian Cells ◽  
Growth Control ◽  
Signal Transduction Pathway ◽  
Negative Control ◽  
Transduction Pathway ◽  
Aba Signal Transduction ◽  
Experimental Approaches ◽  
Main Components

Abscisic acid (ABA) mediated growth control is a fundamental response of plants to adverse environmental cues. The linkage between ABA perception and growth control is currently being unravelled by using different experimental approaches such as mutant analysis and microinjection experiments. So far, two protein phosphatases, ABI1 and ABI2, cADPR, pH and Ca 2+ have been identified as main components of the ABA signalling pathway. Here, the ABA signal transduction pathway is compared to signalling cascades from yeast and mammalian cells. A model for a bifurcated ABA signal transduction pathway exerting a positive and negative control mechanism is proposed.

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