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Genetic redundancy occurs when overlapping functions of different genes allow one to compensate for loss of another under specified conditions. A normal-looking single mutant can therefore conceal an important contribution to a process.

For a toy model, let $a,b\in \{0,1\}$ indicate whether either of two sufficient functions is present. The outputis $1$ for $(a,b)=(1,1),(1,0),(0,1)$ and $0$ only for $(0,0)$. This is a Boolean disjunction model of compensation, not a claim that all biological effects are binary.

The SHATTERPROOF genes give an experimental example. Individual SHATTERPROOF1 or SHATTERPROOF2 disruptions did not produce the novel opening defect detected in the double mutant, connecting overlapping regulatory functions to fruit dehiscence.^[ref]

The conclusion is conditional on the measured phenotype and environment. Compensation for opening a fruit does not establish identical gene expression, identical DNA sequences or interchangeability in every tissue.

Sarah J. Liljegren is a researcher in plant development and genetics. In a 2000 collaborative study, she investigated how the SHATTERPROOF genes SHATTERPROOF1 and SHATTERPROOF2 control fruit dehiscence, the opening of a mature fruit that releases its seeds. These genes encode MADS-box transcription factors and help specify the tissues where the fruit opens.^[ref]

The comparison between single and double mutants is illuminating. Disabling either SHATTERPROOF1 or SHATTERPROOF2 alone produced no new visible phenotype, while disrupting both impaired normal fruit dehiscence. This is an example of genetic redundancy: an experiment on only one gene could miss a shared developmental function. The combined mutant and constitutive-expression experiments connected these genes with the differentiation of the opening zone and lignin deposition in neighboring cells, linking gene activity to the mechanics of seed dispersal.^[ref]

The SHATTERPROOF genes are the related Arabidopsis thaliana genes SHATTERPROOF1 and SHATTERPROOF2, encoding MADS-box transcription factors involved in fruit dehiscence. Their developmental role connects regulation of gene expression to formation of the dehiscence zone and adjacent lignin deposition.^[ref]

The paired experiment matters. Compare the normal plant, each single mutant, and the double mutant. An effect appearing chiefly in the last comparison supplies evidence for genetic redundancy; observing only the normal plant and one single mutant could miss the shared function.^[ref]

The family name groups the two loci; it does not identify one fused gene. The opening phenotype also does not by itself enumerate the transcription factors' direct DNA targets. Distinguishing locus identity, regulatory activity and tissue-level outcome makes the experimental claim precise.