To give a new perspective on the evolutionary characteristics shaping the genetic diversity of enterovirus 71 (EV71) and the effects of natural selection from its host on the codon usage pattern of the virus, the relative synonymous codon usage (RSCU) values, codon usage bias (CUB) values, effective number of codons (ENCs) values and nucleotide contents were calculated to implement a comparative analysis to evaluate the dynamics of the virus evolution. The characteristics of the synonymous codon usage patterns and nucleotide contents of EV71 and the comparison between ENC values for the whole coding sequence of EV71 and that of coding sequences for viral proteins of EV71 all indicate that the interaction between mutation pressure from virus and natural selection from host exists in the processes of evolution of EV71. The synonymous codon usage pattern of EV71 is a mixture of coincidence and antagonism to that of host cell. In addition, the genetic diversity of EV71 strains and the preferential selection of some synonymous codons in EV71 strains based on the different epidemic areas were observed, suggesting that geographic and social factors may play roles in influencing the evolution of this virus.
Plant pathogens, such as bacteria, fungi, oomycetes and nematodes, rely on wide range of virulent effectors delivered into host cells to suppress plant immunity. Although phytobacterial effectors have been intensively investigated, little is known about the function of effectors of plant-parasitic nematodes, such as
Globodera pallida
, a cyst nematode responsible for vast losses in the potato and tomato industries. Here, we demonstrate using
in vivo
and
in vitro
ubiquitination assays the potato cyst nematode (
Globodera pallida
) effector RHA1B is an E3 ubiquitin ligase that employs multiple host plant E2 ubiquitin conjugation enzymes to catalyze ubiquitination. RHA1B was able to suppress effector-triggered immunity (ETI), as manifested by suppression of hypersensitive response (HR) mediated by a broad range of nucleotide-binding leucine-rich repeat (NB-LRR) immune receptors, presumably via E3-dependent degradation of the NB-LRR receptors. RHA1B also blocked the flg22-triggered expression of
Acre31
and
WRKY22
, marker genes of pathogen‐associated molecular pattern (PAMP)‐triggered immunity (PTI), but this did not require the E3 activity of RHA1B. Moreover, transgenic potato overexpressing the
RHA1B
transgene exhibited enhanced susceptibility to
G
.
pallida
. Thus, our data suggest RHA1B facilitates nematode parasitism not only by triggering degradation of NB-LRR immune receptors to block ETI signaling but also by suppressing PTI signaling via an as yet unknown E3-independent mechanism.
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