A geminivirus satellite protein manipulates expressions of NbbZIP60 and its downstream genes to benefit virus infection (IMAGE)
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Geminivirus invasion triggers endoplasmic reticulum (ER) stress and activates the unfolded protein response (UPR). Then the activated NbbZIP60 regulates the expression of its downstream genes in the nucleus, including pro-survival genes (e.g., BiP and CRT), pro-death genes (e.g., NAC089), and other defense genes. Geminivirus satellite βC1 can exploit NbbZIP60 and the chaperons such as BiP and CRT to increase protein accumulations in the early stage of infection. However, accumulating aggregated viral proteins in ER might cause severe ER stresses, leading to cell death. Therefore, βC1 needs to elicit the nuclear export of NbbZIP60 in the late stage of infection through the XPO1 pathway to balance viral protein accumulation and ER stress to create a favourable environment for virus survival and multiplication.
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