Precambrian origins of the TNFR superfamily

Quistad, Steven D.; Traylor-Knowles, Nikki

doi:10.1038/cddiscovery.2016.58

Cited by 36 publications

(31 citation statements)

References 54 publications

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“…S.rosetta contains only 9411 genes, out of which 2 faim genes were found 11 . This evidence suggests that the faim gene evolved much earlier than many other genes and domains found in multicellular organisms, including the death domain involved in animal cell apoptosis [12][13][14] , and implies that this gene may have another major function beyond apoptosis regulation. However, a lack of known consensus effector/binding motifs and even partial sequence homology of FAIM with any other protein has to date rendered it difficult to predict such functions 7 .…”

Section: Introductionmentioning

confidence: 95%

FAIM opposes stress-induced loss of viability and blocks the formation of protein aggregates

Kaku

2019

Preprint

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A number of proteinopathies are associated with accumulation of misfolded proteins, which form pathological insoluble deposits. It is hypothesized that molecules capable of blocking formation of such protein aggregates might avert disease onset or delay disease progression. Here we report that Fas Apoptosis Inhibitory Molecule (FAIM) counteracts stress-induced loss of viability. We found that levels of ubiquitinated protein aggregates produced by cellular stress are much greater in FAIM-deficient cells and tissues. Moreover, in an in vitro cell-free system, FAIM specifically and directly prevents pathological protein aggregates without participation by other cellular elements, in particular the proteasomal and autophagic systems. Although this activity is similar to the function of heat shock proteins (HSPs), FAIM, which is highly conserved throughout evolution, bears no homology to any other protein, including HSPs. These results identify a new actor that protects cells against stress-induced loss of viability by preventing protein aggregates.

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Section: Introductionmentioning

confidence: 95%

FAIM opposes stress-induced loss of viability and blocks the formation of protein aggregates

Kaku

2019

Preprint

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“…Additionally, FosB can be active on its own and has been linked to functions in the extracellular matrix control of smooth muscle cells (Ramachandran et al, 2011). TNFR41 is part of the TNFR family, which was previously found to be highly upregulated in response to heat in corals (Barshis et al, 2013;Quistad et al, 2013Quistad et al, , 2014Quistad and Traylor-Knowles, 2016;Traylor-Knowles and Palumbi, 2014), and its role in other organisms includes activating signaling pathways leading to apoptosis or to proliferation of cells (Aggarwal, 2003;Cabal-Hierro and Lazo, 2012;Gaur and Aggarwal, 2003;MacEwan, 2002). Fig.…”

Section: Induction Of Expression For Genes Chosen For In Situ Analysismentioning

confidence: 99%

“…Untangling the TNFR signaling mechanisms in corals will be challenging. There are many different types (42 in total) and they possess rich sequence diversity (Quistad and Traylor-Knowles, 2016). …”

Section: The Role Of Tnfrs In Heat Stressmentioning

confidence: 99%

“…Additionally, module 1 was identified as being highly enriched for a large number of general stress response-like genes, including tumor necrosis factor receptor (TNFR) genes (Rose et al, 2015). The TNFR gene family has recently been identified as having significant upregulation in corals exposed to heat stress but the actual function and localization of this gene response within the coral animal is still not understood (Barshis et al, 2013;Quistad and Traylor-Knowles, 2016;Quistad et al, 2014). Throughout the continuation of this article, we will refer to module 1 as the 'stress response module' and module 12 as the 'bleaching module'.…”

Section: Introductionmentioning

confidence: 99%

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The cell specificity of gene expression in the response to heat stress in corals

Traylor-Knowles

Rose

Palumbi

2017

Journal of Experimental Biology

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Previous transcriptional studies in heat-stressed corals have shown that many genes are responsive to generalized heat stress whereas the expression patterns of specific gene networks after heat stress show strong correlations with variation in bleaching outcomes. However, where these specific genes are expressed is unknown. In this study, we employed in situ hybridization to identify patterns of spatial gene expression of genes previously predicted to be involved in general stress response and bleaching. We found that tumor necrosis factor receptors (TNFRs), known to be strong responders to heat stress, were not expressed in gastrodermal symbiont-containing cells but were widely expressed in specific cells of the epidermal layer. The transcription factors AP-1 and FosB, implicated as early signals of heat stress, were widely expressed throughout the oral gastrodermis and epidermis. By contrast, a G protein-coupled receptor gene (GPCR) and a fructose bisphosphate aldolase C gene (aldolase), previously implicated in bleaching, were expressed in symbiont-containing gastrodermal cells and in the epidermal tissue. Finally, chordin-like/kielin (chordin-like), a gene highly correlated to bleaching, was expressed solely in the oral gastrodermis. From this study, we confirm that heat-responsive genes occur widely in coral tissues outside of symbiont-containing cells. Joint information about expression patterns in response to heat and cell specificity will allow greater dissection of the regulatory pathways and specific cell reactions that lead to coral bleaching.

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“…Many versions of apoptosis exist (Holler et al, 2000;Berg et al, 2001;Bratosin et al, 2001) and the general process likely emerged with the origin of multicellularity (Ellis and Horvitz, 1986;Raff, 1992;Steller, 1995;Aravind et al, 2001). However, metazoan apoptosis appears to be unique through its use of TNF receptors (Quistad and Traylor-Knowles, 2016), which are activated by TNF ligands (Aggarwal, 2003). Many of the domains involved with apoptotic signaling via TNF receptors are also present and functional in cnidarians, considered to be among the oldest animal phyla (Lasi et al, 2010;Quistad et al, 2014;Sakamaki et al, 2014Sakamaki et al, , 2015Lu et al, 2016;Moya et al, 2016).…”

Section: Tumor Necrosis Factor (Tnf)-induced Apoptosis-an Internal MImentioning

confidence: 99%

Viruses and the origin of microbiome selection and immunity

et al. 2016

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The last common metazoan ancestor (LCMA) emerged over half a billion years ago. These complex metazoans provided newly available niche space for viruses and microbes. Modern day contemporaries, such as cnidarians, suggest that the LCMA consisted of two cell layers: a basal endoderm and a mucus-secreting ectoderm, which formed a surface mucus layer (SML). Here we propose a model for the origin of metazoan immunity based on external and internal microbial selection mechanisms. In this model, the SML concentrated bacteria and their associated viruses (phage) through physical dynamics (that is, the slower flow fields near a diffusive boundary layer), which selected for mucin-binding capabilities. The concentration of phage within the SML provided the LCMA with an external microbial selective described by the bacteriophage adherence to mucus (BAM) model. In the BAM model, phage adhere to mucus protecting the metazoan host against invading, potentially pathogenic bacteria. The same fluid dynamics that concentrated phage and bacteria in the SML also concentrated eukaryotic viruses. As eukaryotic viruses competed for host intracellular niche space, those viruses that provided the LCMA with immune protection were maintained. If a resident virus became pathogenic or if a non-beneficial infection occurred, we propose that tumor necrosis factor (TNF)-mediated programmed cell death, as well as other apoptosis mechanisms, were utilized to remove virally infected cells. The ubiquity of the mucosal environment across metazoan phyla suggest that both BAM and TNF-induced apoptosis emerged during the Precambrian era and continue to drive the evolution of metazoan immunity.

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Precambrian origins of the TNFR superfamily

Cited by 36 publications

References 54 publications

FAIM opposes stress-induced loss of viability and blocks the formation of protein aggregates

FAIM opposes stress-induced loss of viability and blocks the formation of protein aggregates

The cell specificity of gene expression in the response to heat stress in corals

Viruses and the origin of microbiome selection and immunity

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