As sessile organisms, plants face a variety of environmental challenges. Their reproduction and survival depend on their ability to adapt to these stressors, which include water, heat stress, high salinity, and pathogen infection. Failure to adapt to these stressors results in programmed cell death and decreased viability, as well as reduced productivity in the case of crop plants. The growth and development of plants are maintained by meiosis and mitosis as well as endoreduplication, during which DNA replicates without cytokinesis, leading to polyploidy. As in other eukaryotes, the cell cycle in plants consists of four stages (G1, S, G2, and M) with two major check points, namely, the G1/S check point and G2/M check point, that ensure normal cell division. Progression through these checkpoints involves the activity of cyclin-dependent kinases and their regulatory subunits known as cyclins. In order for plants to survive, cell cycle control must be balanced with adaption to dynamic environmental conditions. In this review, we summarize recent advances in our understanding of cell cycle regulation in plants, with a focus on the molecular interactions of cell cycle machinery in the context of stress tolerance. FIGURE 1 | Schematic representation of the mitotic cell cycle in plants.At the G1 phase, D-type cyclins (CYCD) interact with the A-type CDK (CDKA), forming the CDKA/CYCD complex. The activity of CDKA/CYCD complex can be negatively regulated by KPR and SIM proteins. Once activation, this complex phosphorylates RBR to release the transcript factor E2Fa/b-DP. This E2Fa/b-DP complex binds to the E2F box and activate the transcription of S phase genes. At the G2 and M phase S, CYCA and CYCB are strongly expressed and their gene products assemble with CDKA and CDKB. The CYCD can also associate with CDKs. At the beginning of G2 phase, CDK activity are inhibited because of the phosphorylation of Y14 and T15 site by WEEI kinase. The CDC25-related kinase, which removes the inhibitory phosphate groups, still needs to be identified. Once the CDK/CYC complex are active, they phosphorylate MYB3R transcription factors and activate mitotic genes' transcription. Mitotic exit requires anaphase-promoting complex (APC), which degrades cyclins through ubiquitin-proteasome pathway.