Final answer:
A mutation that stops programmed cell death can cause cells to revert to a reproductive state, similar to the effect of a mutated p53 gene in humans, which can lead to tumor growth.
Step-by-step explanation:
A mutation in a gene that abolishes programmed cell death in organisms like Volvox can lead to cells dedifferentiating into a reproductive state (gonidia) instead of dying. This phenomenon is similar to what happens when human cells experience a mutation in the p53 gene.
Normally, p53 functions at the G₁ checkpoint to halt the cell cycle for DNA repair, or to initiate cell death (apoptosis) if the damage is irreparable.
A faulty p53 gene might fail to detect DNA errors or signal the repair mechanisms, allowing damaged cells to divide, thus propagating mutations and possibly leading to tumor growth due to the accumulation of oncogenes and non-functional tumor suppressor genes.