Paternal Effects in Inheritance of a Pathogen Resistance Trait in Ipomoea purpurea

Evolution ◽  
1996 ◽  
Vol 50 (6) ◽  
pp. 2178 ◽  
Author(s):  
Ellen L. Simms ◽  
Jim K. Triplett
2018 ◽  
Author(s):  
Rudolf Fullybright

Accurate quantification of biological resistance has been impossible so far. Among the various forms of biological resistance which exist in nature, pathogen resistance to drugs is a familiar one. However, as in the case of other forms of resistance, accurately quantifying drug resistance in pathogens has been impossible up to now. Here, we introduce a mathematically-defined and uniform procedure for the absolute quantification of biological resistance deployed by any living organism in the biological realm, including and beyond drug resistance in medicine. The scheme introduced makes possible the exact measurement or computation of the extent to which resistance is deployed by any living organism regardless of kingdom and regardless of the mechanism of resistance involved. Furthermore, the Second Law of Resistance indicating that resistance has the potential to increase to infinite levels, and the Third Law of Resistance indicating that resistance comes to an end once interaction stops, the resistance unit function introduced here is fully compatible with both the Second and Third Laws of Resistance.


2020 ◽  
Vol 40 (8) ◽  
Author(s):  
Fayang Liu ◽  
Hongni Xue ◽  
Jie Ke ◽  
Yongyan Wu ◽  
Kezhen Yao ◽  
...  

ABSTRACT Intracellular pathogen resistance 1 (Ipr1) has been found to be a mediator to integrate cyclic GMP-AMP synthase (cGAS)–interferon regulatory factor 3 (IRF3), activated by intracellular pathogens, with the p53 pathway. Previous studies have shown the process of Ipr1 induction by various immune reactions, including intracellular bacterial and viral infections. The present study demonstrated that Ipr1 is regulated by the cGAS-IRF3 pathway during pathogenic infection. IRF3 was found to regulate Ipr1 expression by directly binding the interferon-stimulated response element motif of the Ipr1 promoter. Knockdown of Ipr1 decreased the expression of immunity-related GTPase family M member 1 (Irgm1), which plays critical roles in autophagy initiation. Irgm1 promoter characterization revealed a p53 motif in front of the transcription start site. P53 was found to participate in regulation of Irgm1 expression and IPR1-related effects on P53 stability by affecting interactions between ribosomal protein L11 (RPL11) and transformed mouse 3T3 cell double minute 2 (MDM2). Our results indicate that Ipr1 integrates cGAS-IRF3 with p53-modulated Irgm1 expression.


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