The process of cell division requires a precise choreography of events to ensure genetic material is duplicated and distributed correctly. At the heart of this process are two related protein complexes, condensin and cohesin, which organize DNA. Both belong to a larger family of proteins known as Structural Maintenance of Chromosomes (SMC) complexes. This shared ancestry gives them a similar core architecture, yet they perform distinct functions timed to specific phases of the cell cycle. Understanding their individual roles is the first step in appreciating how they work together to facilitate one of life’s most basic processes.
Cohesin and Sister Chromatid Cohesion
Cohesin’s primary role is to act as molecular glue. After DNA replication during the S phase, the cell has two identical copies of each chromosome, known as sister chromatids. Cohesin holds these sister chromatids together along their entire length. Its ring-like structure, composed of four protein subunits, physically encircles the pair of chromatids to tether them.
This tethering is important for the accuracy of cell division. By keeping the sister chromatids paired, cohesin ensures the chromosomes are correctly organized and aligned for division. This pairing allows the cell’s machinery to attach to the chromosomes properly, so each new daughter cell receives a complete set of genetic instructions. This cohesion is established during DNA replication and maintained through the early stages of mitosis.
Cohesin’s role ends with an abrupt release. As the cell transitions into anaphase, the cohesin rings are broken. This cleavage allows the sister chromatids to separate and be pulled to opposite ends of the cell. The removal of cohesin is a highly regulated event, signaling that the cell is ready to complete its division into two genetically identical daughter cells.
Condensin and Chromosome Compaction
While cohesin holds sister chromatids together, condensin organizes the structure of each individual chromatid. In their normal state, DNA strands are extremely long and thin. Condensin’s function is to compact these lengthy strands into shorter, denser structures that are manageable for segregation during mitosis. This compaction makes chromosomes visible under a light microscope.
Condensin achieves this compaction through the “loop extrusion” model. The condensin complex latches onto a DNA strand and actively reels it in, forming a series of loops. This process shortens and thickens the chromatid, similar to winding a long thread around a spool. This activity increases as the cell enters prophase, the first stage of mitosis.
Two types of condensin complexes, condensin I and condensin II, work together to shape mitotic chromosomes. Condensin II is found within the nucleus and initiates the early stages of compaction. As the nuclear envelope breaks down in prophase, condensin I gains access to the chromosomes from the cytoplasm. It then contributes to the final, highly compacted state seen in metaphase.
Coordination During Cell Division
The actions of cohesin and condensin are precisely coordinated throughout mitosis to ensure successful chromosome segregation. Their sequential functions create the iconic chromosomal structures observed during cell division. Cohesin is loaded onto the DNA during replication in the S phase, well before mitosis begins.
As the cell enters prophase, condensin complexes begin their work. They bind to the chromatids already held together by cohesin and start the compaction process. During prophase, chromosomes are simultaneously shortened by condensin while being held in pairs by cohesin, preparing them for the next stage.
By metaphase, chromosomes reach maximum compaction and align at the cell’s equator. This creates a lineup of X-shaped structures, each consisting of two condensed sister chromatids linked by cohesin. This alignment is a checkpoint, ensuring each chromatid is attached to the mitotic spindle, the machinery that will pull them apart. The resulting tension signals that the cell is ready to proceed.
The transition to anaphase is triggered by the removal of cohesin. An enzyme called separase cleaves the cohesin complex, breaking the rings holding the sister chromatids together. Once liberated, the individual, condensed chromosomes are pulled to opposite poles of the cell by spindle fibers. This ensures each daughter cell receives a full complement of genetic material.
Consequences of Malfunction
Errors in cohesin or condensin function can have severe consequences. If these complexes do not work correctly, chromosomes may not be properly compacted or separated. This can result in aneuploidy, a condition where daughter cells receive an incorrect number of chromosomes, which is associated with developmental disorders and cancer.
Defects in the genes encoding these complexes cause genetic disorders known as “cohesinopathies” and “condensinopathies.” These conditions highlight the impact of proper chromosome architecture on human health.
Cohesinopathies are more extensively studied, with Cornelia de Lange syndrome being a well-known example. This syndrome results from mutations in genes encoding cohesin components. The faulty cohesin leads to a wide range of developmental issues, including growth delays, intellectual disabilities, and characteristic facial features. The existence of such disorders underscores how the molecular task of holding chromosomes together is connected to the healthy development of an entire organism.