Tale of transposons, HGT and integrated viruses
Title: "Tale of transposons, HGT and integrated viruses."
The journal article "FicD genes in invertebrates: a tale of transposons, pathogenic and integrated viruses" by Rosani et al. (2023) discusses the presence of FicD genes in invertebrates, their potential origins, and their possible roles in viral infection.
FicD genes encode a family of proteins that catalyze AMPylation, a post-translational modification that involves the addition of adenosine monophosphate (AMP) to target proteins. AMPylation is a diverse process with a wide range of functions, including protein signaling, regulation, and degradation.
FicD genes are well-known to be conserved in deuterostomes, which are a group of animals that includes vertebrates, but their presence in invertebrates has been less well-studied. In their article, they report the presence of a conserved FicD gene ortholog in a large number of protostomes and microbial eukaryotes, including insects, mollusks, and worms. They also report additional FicD gene copies in the genomes of some rotifers, parasitic worms, and bivalves.
Interestingly, they also found that a few dsDNA viruses of these invertebrates, including White spot syndrome virus, Cherax quadricarinatus iridovirus, Ostreid herpesvirus-1, and the beetle nudivirus, carry copies of FicDs. Phylogenetic analysis suggested a common origin of these FicD copies and the duplicated FicDs of their invertebrate hosts.
Based on their findings, they propose that horizontal gene transfer (HGT) and gene duplications possibly mediated by endogenous viruses or genetic mobile elements may have contributed to the transfer of AMPylation ability from bacteria and eukaryotes to pathogenic viruses. They also suggest that viruses may have hijacked this pathway to promote viral infection.
In addition to the potential role of FicDs in viral infection, Rosani et al also discuss other possible functions of FicDs in invertebrates. For example, they suggest that FicDs may be involved in innate immunity, host-pathogen interactions, and development.
Overall, the article provides new insights into the distribution and evolution of FicD genes in invertebrates, and suggests a possible role for FicDs in viral infection. This research could have implications for the development of new antiviral therapies.
Here are some additional thoughts on the potential role of FicDs in viral infection:
Viruses are known to manipulate a variety of host cell processes to their advantage. It is possible that viruses that encode FicDs could use these proteins to suppress host immune responses, promote viral replication, or interfere with other host cell processes that are essential for viral infection.
FicD proteins have been shown to interact with a variety of host cell proteins. It is possible that viruses could exploit these interactions to promote viral infection. For example, viruses could encode FicDs that target specific host cell proteins for AMPylation, which could alter their function or localization.
FicD proteins have also been shown to be involved in the regulation of autophagy, a cellular process that is involved in the degradation of damaged proteins and organelles. Autophagy can play a role in both antiviral and antiviral defense. It is possible that viruses could encode FicDs to manipulate autophagy in order to promote viral infection.
Key points of the article:
Horizontal gene transfer (HGT) is a common evolutionary process that can lead to the sharing of gene families between distantly related species.
The frequency of HGTs varies between gene families and biotic realms, suggesting that there is differential selection pressure and functional bias.
The FicD gene family is a well-known example of a gene family that has been conserved across the "Bush of Life" through HGT.
There is no proof of a Darwinian "Tree of Life." FicD gene orthologs have been found in deuterostomes, protostomes, microbial eukaryotes, and even dsDNA viruses.
The analysis of FicD gene sequences suggests that the FicD copies in dsDNA viruses have a common origin with the duplicated FicDs of their invertebrate hosts.
HGTs and gene duplications mediated by endogenous viruses or genetic mobile elements may have contributed to the transfer of AMPylation ability from bacteria and eukaryotes to pathogenic viruses.
The article also suggests that the AMPylation pathway may have been hijacked by pathogenic viruses to promote viral infection. This is an interesting hypothesis, and it would be interesting to see more research on this topic.
Overall, the article provides a good overview of the role of HGT in the evolution of the FicD gene family and the AMPylation pathway. It also highlights the potential role of endogenous viruses and genetic mobile elements in mediating HGTs and gene duplications.
The facts of the article challenges Neo-Darwinism in a few ways.
First, the article shows that FicD genes, which are important for AMPylation, are present in a wide range of invertebrates, including some that are phylogenetically distant from each other. This suggests that FicD genes may have been transferred between different invertebrate species through horizontal gene transfer (HGT). HGT is a process in which genetic material is transferred between organisms that are not closely related. Neo-Darwinism does not account for HGT, as it assumes that evolution is driven solely by natural selection acting on slow random mutations. HGT is rapid where "chunks of DNA can be passed in one generation.
Second, the article shows that some FicD genes are present in the genomes of viruses that infect invertebrates. This suggests that these viruses may have acquired FicD genes from their invertebrate hosts. This is another example of HGT, and it challenges the Neo-Darwinian view that evolution is a unidirectional process from lower to higher organisms.
Third, the article shows that some FicD genes are integrated into the genomes of invertebrates. This means that these genes are now part of the invertebrate genome and are passed on to the next generation. Integration of viral genes into the host genome is known as viral integration, and it is a common way that viruses can manipulate their hosts. Neo-Darwinism does not account for viral integration, as it assumes that evolution is driven solely by natural selection acting on slow mutations. These findings suggest that evolution is a more complex process than Neo-Darwinism allows for.
The information of this article suggests that Neo-Darwinism may need to be modified or replaced to account for the role of HGT and viral integration in evolution.
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