In rod-shaped Gram-negative bacteria, FtsZ localization at midcell position is regulated by the gradient of MinCDE complex across the poles. In round-shaped bacteria, which lack prede fined poles, the next plane of cell division is perpendicular to the previous  plane,  and  determination  of  the  FtsZ  assembly  site  is  still  intriguing. Deinococcus radiodurans, a coccus bacterium, is characterized by its extraordinary resistance to DNA damage. DivIVA, a putative component of the Min system in this bacterium, interacts with cognate cell division and genome segregation proteins. Here, we report that deletion of a chromosomal copy of DivIVA was possible only when the wild-type copy of DivIVA was expressed in trans on a plasmid. However, deletion of the C-terminal domain (CTD) of DivIVA (CTD mutant) was possible but produced distinguishable phenotypes, like smaller cells, slower growth, and tilted septum orientation, in D. radiodurans .In trans expression of DivIVA in the CTD mutant could restore these features of the wild type. Interestingly, the overexpression of DivIVA led to delayed separation of tet-rads from an octet state in both trans -complemented divIVA -mutant and wild-type cells. The CTD mutant showed upregulation of the yggS-divIVAN operon. Both the wild type and CTD mutant formed FtsZ foci; however, unlike wild type, the position of foci in the mutant cells was found to be away from conjectural midcell position in cocci. Notably, DivIVA-red fluorescent protein (DivIVA-RFP) localizes to the septum during cell division at the new division site. These results suggested that DivIVA is an essential protein in D. radiodurans, and its C-terminal domain plays an important role in the regulation of its expression and orientation of new septal growth in this bacterium.