Strategies for geminivirus DNA replication and cell cycle interference [Review]

摘要

Geminivirus DNA replication, and also other steps during infection, rely heavily on the activity of cellular factors. One of the primary events seems to be the inactivation of the RBR protein, that negatively regulates the G1/S transition in cells. This strategy is similar in many respects to that used by animal oncoviruses as it depends on the interaction of certain geminivirus proteins with RBR. It seems that two mechanisms exist. One depends on a viral protein containing the LxCxE motif (for example, mastrevirus RepA and also the nanovirus Clink protein) and the other on two viral proteins lacking this motif, begomovirus Rep and REn. Additional interactions with other cell growth regulatory factors, which are just beginning to be uncovered, are also likely to be important. Activation of the geminivirus origin of DNA replication depends on the interaction of the initiator Rep protein with the origin, which has a characteristic modular structure. Different organizations of the DNA sequence motifs, and unique DNA-protein interactions, occur in mastreviruses and begomoviruses (curtoviruses and the only topocuvirus probably resemble begomoviruses). The variant strategies used by different geminiviruses to impinge on the cell cycle and to assemble protein complexes at the site of the origin of DNA replication are discussed.