There is a problem completing the replication of linear chromosomes at their ends. Describe the problem and identify why telomeres shorten in each replication cycle.

Verified step by step guidance

1. <insert step 1> The problem with replicating linear chromosomes is that DNA polymerase can only add nucleotides to the 3' end of a pre-existing chain, requiring a primer to initiate synthesis.>
2. <insert step 2> During replication, the leading strand is synthesized continuously, but the lagging strand is synthesized in short fragments called Okazaki fragments, each requiring a new primer.>
3. <insert step 3> At the very end of the lagging strand, once the final RNA primer is removed, there is no upstream 3' end available for DNA polymerase to fill in the gap, leading to a short, unreplicated segment.>
4. <insert step 4> This unreplicated segment results in the progressive shortening of the chromosome ends, known as telomeres, with each cell division.>
5. <insert step 5> Telomeres are repetitive nucleotide sequences that protect the ends of chromosomes, but as they shorten with each replication cycle, they eventually reach a critical length that can trigger cellular senescence or apoptosis.>

Key Concepts

Telomeres

Telomeres are repetitive nucleotide sequences located at the ends of linear chromosomes. They protect the chromosome from deterioration or fusion with neighboring chromosomes. Each time a cell divides, a portion of the telomere is not replicated, leading to gradual shortening over successive replication cycles.

DNA Replication

DNA replication is the process by which a cell duplicates its DNA before cell division. It involves unwinding the double helix and synthesizing new strands complementary to the original ones. However, due to the nature of DNA polymerase, which cannot fully replicate the ends of linear chromosomes, telomeres become progressively shorter with each replication.

Hayflick Limit

The Hayflick limit refers to the number of times a normal somatic human cell can divide before cell division stops, which is typically around 40-60 divisions. This limit is largely due to telomere shortening, as critically short telomeres trigger cellular senescence or apoptosis, preventing further replication and contributing to aging and tissue regeneration limitations.