$"$In epithelial cells, tight junctions are essential for creating a selective barrier. Given that the scaffolding protein ZO$-1$ localizes to the junction before claudin and occludin proteins are fully assembled, yet knockout studies show that cells lacking claudins fail to recruit ZO$-1$ to cell$-$cell contacts, and considering that occludin$-$deficient cells can still form partially functional tight junctions despite reduced barrier integrity, what evolutionary explanation resolves this apparent paradox in the sequential assembly of tight junction components?"