scholarly journals Chemosensory Neurons Modulate the Response to Oomycete Recognition in Caenorhabditis elegans

Cell Reports ◽  
2021 ◽  
Vol 34 (2) ◽  
pp. 108604
Author(s):  
Michael K. Fasseas ◽  
Manish Grover ◽  
Florence Drury ◽  
Clara L. Essmann ◽  
Eva Kaulich ◽  
...  
Neuroreport ◽  
2000 ◽  
Vol 11 (10) ◽  
pp. 2229-2232 ◽  
Author(s):  
Yoshihiro Sambongi ◽  
Kenji Takeda ◽  
Tokumitsu Wakabayashi ◽  
Ikuo Ueda ◽  
Yoh Wada ◽  
...  

2020 ◽  
Vol 295 (50) ◽  
pp. 17323-17336
Author(s):  
Jinyuan Yan ◽  
Ninghui Zhao ◽  
Zhongshan Yang ◽  
Yuhong Li ◽  
Hua Bai ◽  
...  

Recent studies have suggested that innate immune responses exhibit characteristics associated with memory linked to modulations in both vertebrates and invertebrates. However, the diverse evolutionary paths taken, particularly within the invertebrate taxa, should lead to similarly diverse innate immunity memory processes. Our understanding of innate immune memory in invertebrates primarily comes from studies of the fruit fly Drosophila melanogaster, the generality of which is unclear. Caenorhabditis elegans typically inhabits soil harboring a variety of fatal microbial pathogens; for this invertebrate, the innate immune system and aversive behavior are the major defensive strategies against microbial infection. However, their characteristics of immunological memory remains infantile. Here we discovered an immunological memory that promoted avoidance and suppressed innate immunity during reinfection with bacteria, which we revealed to be specific to the previously exposed pathogens. During this trade-off switch of avoidance and innate immunity, the chemosensory neurons AWB and ADF modulated production of serotonin and dopamine, which in turn decreased expression of the innate immunity-associated genes and led to enhanced avoidance via the downstream insulin-like pathway. Therefore, our current study profiles the immune memories during C. elegans reinfected by pathogenic bacteria and further reveals that the chemosensory neurons, the neurotransmitter(s), and their associated molecular signaling pathways are responsible for a trade-off switch between the two immunological memories.


Lab on a Chip ◽  
2010 ◽  
Vol 10 (20) ◽  
pp. 2758 ◽  
Author(s):  
Trushal Vijaykumar Chokshi ◽  
Daphne Bazopoulou ◽  
Nikos Chronis

2002 ◽  
Vol 189 (1) ◽  
pp. 55-66 ◽  
Author(s):  
W.T. Nickell ◽  
R.Y.K. Pun ◽  
C.I. Bargmann ◽  
S.J. Kleene

2020 ◽  
Vol 24 (8) ◽  
Author(s):  
Jinyang Chung ◽  
Christopher A. Brittin ◽  
Stephen D. Evans ◽  
Netta Cohen ◽  
Jung-uk Shim

Genetics ◽  
1995 ◽  
Vol 139 (1) ◽  
pp. 171-188 ◽  
Author(s):  
T A Starich ◽  
R K Herman ◽  
C K Kari ◽  
W H Yeh ◽  
W S Schackwitz ◽  
...  

Abstract We have identified and characterized 95 mutations that reduce or abolish dye filling of amphid and phasmid neurons and that have little effect on viability, fertility or movement. Twenty-seven mutations occurred spontaneously in strains with a high frequency of transposon insertion. Sixty-eight were isolated after treatment with EMS. All of the mutations result in defects in one or more chemosensory responses, such as chemotaxis to ammonium chloride or formation of dauer larvae under conditions of starvation and overcrowding. Seventy-five of the mutations are alleles of 12 previously defined genes, mutations which were previously shown to lead to defects in amphid ultrastructure. We have assigned 20 mutations to 13 new genes, called dyf-1 through dyf-13. We expect that the genes represented by dye-filing defective mutants are important for the differentiation of amphid and phasmid chemosensilla.


1999 ◽  
Vol 147 (3) ◽  
pp. 519-530 ◽  
Author(s):  
Dawn Signor ◽  
Karen P. Wedaman ◽  
Jose T. Orozco ◽  
Noelle D. Dwyer ◽  
Cornelia I. Bargmann ◽  
...  

The heterotrimeric motor protein, kinesin-II, and its presumptive cargo, can be observed moving anterogradely at 0.7 μm/s by intraflagellar transport (IFT) within sensory cilia of chemosensory neurons of living Caenorhabditis elegans, using a fluorescence microscope–based transport assay (Orozco, J.T., K.P. Wedaman, D. Signor, H. Brown, L. Rose, and J.M. Scholey. 1999. Nature. 398:674). Here, we report that kinesin-II, and two of its presumptive cargo molecules, OSM-1 and OSM-6, all move at ∼1.1 μm/s in the retrograde direction along cilia and dendrites, which is consistent with the hypothesis that these proteins are retrieved from the distal endings of the cilia by a retrograde transport pathway that moves them along cilia and then dendrites, back to the neuronal cell body. To test the hypothesis that the minus end–directed microtubule motor protein, cytoplasmic dynein, drives this retrograde transport pathway, we visualized movement of kinesin-II and its cargo along dendrites and cilia in a che-3 cytoplasmic dynein mutant background, and observed an inhibition of retrograde transport in cilia but not in dendrites. In contrast, anterograde IFT proceeds normally in che-3 mutants. Thus, we propose that the class DHC1b cytoplasmic dynein, CHE-3, is specifically responsible for the retrograde transport of the anterograde motor, kinesin-II, and its cargo within sensory cilia, but not within dendrites.


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