Geminiviruses cause devastating diseases in fields and economic losses in agriculture in the world, they induce severe developmental abnormalities in plants. Geminivirus-encoded C4 protein functions as one of viral symptom determinants that could induce abnormal cell division. However, the molecular mechanism by which C4 contributes to cell division induction remains unclear. Recently, a research group led by Prof. Zhou Xueping at the Department of Biotechnology in Plant Protection published a research paper in PloS Pathogens providing new insights into mechanism of how a viral protein hijacks host protein to induce abnormal cell division in plants. They report that tomato leaf curl Yunnan virus (TLCYnV) C4 interacts with a glycogen synthase kinase 3 (GSK3)/SHAGGY-like kinase, designed NbSKη, in Nicotiana benthamiana. Pro32, Asn34 and Thr35 of TLCYnV C4 are critical for its interaction with NbSKη and required for C4-induced typical symptoms. Interestingly, TLCYnV C4 directs NbSKη to the membrane and reduces the nuclear-accumulation of NbSKη. Moreover, NbSKη-RNAi, 35S::NbCycD1; 1 transgenic N. benthamiana plants have the similar phenotype as 35S:: C4 transgenic N. benthamiana plants on callus-like tissue formation resulted from abnormal cell division induction. C4 hijacks the NbSKη on the membrane to avoid the phosphorylation and proteasomal degradation of nucleus-located NbCycD1;1, and then increase the accumulation level of NbCycD1;1. The biological significance for this relocalization is to reactivate an environment suitable for DNA virus replication in mature and differentiated leaves and induce cell divisions.

More details are available on the bellow links:
http://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1006789