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Ruediger, C.

Publications and source records attributed to Ruediger, C..

2 recordsLinked to original sources

Computational design and experimental characterization of mini-protein binders targeting Nipah, Langya and Measles virus receptor-binding domains

A lack of reagents represents a major bottleneck in pandemic preparedness and rapid vaccine development. It is therefore important to enable the design of reagents for use in the treatment and diagnosis of emerging viral diseases. Ideally, the design and identification platform is fast, can be performed by testing only a small number of candidates and enables a generally applicable strategy. In this study, we assessed the ability of recently developed computational protein design tools to establish such a workflow for validating paramyxovirus receptor-binding protein de novo binders as such reagents. The family Paramyxoviridae includes various members that cause severe disease and exhibit re-occurring zoonotic spillover events, with documented human infections over the past decades. We successfully designed, identified, and characterized mini-proteins targeting the receptor binding proteins of Nipah virus, Langya virus, and Measles virus while screening as few as 10-16 designs per target. The resulting functional binders have moderate to low nanomolar affinities and display high on-target specificity. We further showed that our most promising Nipah virus receptor-binding protein binder is able to inhibit human receptor binding in vitro and competes for an epitope that overlaps with that of the neutralizing antibody HENV-117. However, despite these promising results, this Nipah binder is only weakly neutralizing, preventing therapeutic applications. Nevertheless, we established a platform, applicable to rapidly generate diagnostically relevant proteins from only a small number of candidates, and developed novel reagents for the Paramyxoviridae family.

bioinformatics↗

mir-71 mediates age-dependent opposing contributions of the stress activated kinase KGB-1 in Caenorhabditis elegans

Studying the evolutionary processes that shaped aging offers a path for understanding the causes of aging. The Antagonistic Pleiotropy theory for the evolution of aging proposes that the inverse correlation between natural selection strength and aging allows positive selection of gene variants with early-life beneficial contributions to fitness in spite of detrimental late-life consequences. However, mechanistic understanding of how this principle manifests in aging is still lacking. We previously identified antagonistic pleiotropy in the function of the Caenorhabditis elegans JNK homolog KGB-1, which provided stress protection in developing larvae, but sensitized adults to stress and shortened their lifespan. To a large extent, KGB-1s contributions depended on age-dependent and opposing regulation of the stress transcription factor DAF-16, but the underlying mechanisms remained unknown. Here we describe a role for the microRNA mir-71 in mediating effects of KGB-1 on DAF-16 and on downstream phenotypes. Fluorescent imaging along with genetic and survival analyses revealed age-dependent regulation of mir-71 expression by KGB-1 - upregulation in larvae, but downregulation in adults, and showed that mir-71 was required both for late-life effects of KGB-1 (infection sensitivity and shortened lifespan), as well as for early life resistance to cadmium. While mir-71 disruption did not compromise development under protein folding stress (known to depend on KGB-1), disruption of the argonaute gene alg-1, a central component of the microRNA machinery, did. These results suggest that microRNAs play a role in mediating age-dependent antagonistic contributions of KGB-1 to survival, with mir-71 playing a central role and additional microRNAs contributing redundantly.

genetics↗