On the other hand, chromatin bridges also generated micronuclei in the same cells, and here chromatin was more condensed compared to the main nucleus even after the completion of mitosis. In order to obtain frequencies, we examined many cells that were fixed by PFA in situ. We identified chromatinGrapiprant bridge-derived micronuclei based on the criterion that the bridge usually produced multiple micronuclei or buds, which appear ����in line���� inside the anaphase/telophase cells. The micronuclei that did not pass this criterion were classified as lagging chromatid-derived. Our results suggest that the micronuclei generated from the lagging chromatid generally had more relaxed chromatin than the nucleus, whereas those generated from the bridge had more condensed chromatin. Presence of lamina around micronuclei had previously been correlated to transcription inside micronuclei, which has important implications for cell phenotype. Thus, we imaged presence of lamin B among fixed cells by immunofluorescence. We distinguished chromatin bridge-derived and lagging chromatidderived micronuclei according to the criterion stated above. We found lamin B around lagging chromatid-derived micronucleus but rarely around bridge-derived micronuclei. Another representative image shows a bridge-derived chromatid as condensed and devoid of lamin B while apart from the nucleus, but surrounded by lamin B when connected to the nucleus as a nuclear bud. We recorded the frequency of each type of micronuclei in the fixed and lamin B immunostained cells. The results suggested that the bridge-derived micronuclei were less frequently associated with lamin B protein compared to the lagging chromatid-derived micronuclei. In this study, we have addressed how micronuclei emerge and affect cell fate after replication stress in human cervical cancer cells. We had reported that the same replication stress used here can induce micronuclei in normal cells if p53 is malfunctioning. Therefore, data presented here may also be applicable to p53 negative cells.Here, we found that presence of micronuclei typically resulted in LY2409881 apoptotic cell death but not in multipolar mitosis. There are two possible explanations for these observations: Micronuclei-bearing cells had severe DNA damage that might induce apoptosis. However, cells bearing micronuclei caused multipolar mitosis as rarely as normal cells.