Abstract：
:Dealing with physiological stress is a necessity for all organisms, and the pathways charged with this task are highly conserved in Metazoa . Accumulating evidence highlights cell-nonautonomous activation as an important mode of integrating stress responses at the organism level. Work in Caenorhabditis elegans highlighted the importance of such regulation for the unfolded protein response (UPR) and for gene expression downstream of the longevity-associated transcription factor DAF-16 Here we describe a role for the JNK homolog KGB-1 in cell-nonautonomous regulation of these two response modules. KGB-1 protects developing larvae from heavy metals and from protein folding stress (which we found to be independent of canonical UPR pathways), but sensitizes adults to the same stress, further shortening life span under normal conditions. This switch is associated with age-dependent antagonistic regulation of DAF-16 Using transgenic tissue-specific KGB-1 expression or tissue-specific KGB-1 activation we examined the contributions of KGB-1 to gene regulation, stress resistance, and life span. While cell-autonomous contributions were observed, particularly in the epidermis, cell-nonautonomous contributions of neuronal KGB-1 (and also in muscle) were effective in driving intestinal gene induction, age-dependent regulation of intestinal DAF-16, and stress resistance, and did not require KGB-1 expression in the target tissue. Additional genetic analyses revealed requirement for UNC-13 in mediating neuronal contributions, indicating involvement of neurotransmission. Our results expand the role of KGB-1 in stress responses from providing local cellular protection to integrating stress responses at the level of the whole organism.
journal_name
Geneticsjournal_title
Geneticsauthors
Liu L,Ruediger C,Shapira Mdoi
10.1534/genetics.118.301446subject
Has Abstractpub_date
2018-12-01 00:00:00pages
1317-1328issue
4eissn
0016-6731issn
1943-2631pii
genetics.118.301446journal_volume
210pub_type
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