# Review: gene inactivation shaped adaptation in whales, naked mole-rats, hummingbirds and pandas

- Published: 2026-11-13 16:14 UTC
- Section: Life & Health › Biology & biochemistry
- Tags: pseudogenes, junk DNA, pseudogenization, adaptive evolution, TLR5 in cetaceans, naked mole-rat vision, FBP2 hummingbird, PTENP1, long-read RNA-seq, CRISPR/Cas9 base editing
- URL: https://realtech.media/news/rt-bc0cf647c6a6ed02b72b0003_review_gene_inactivation/

**A review in The Innovation Life collects cases where pseudogenization helped vertebrates adapt, and shows that pseudogene transcripts can protect against or drive human disease.**

![Review: gene inactivation shaped adaptation in whales, naked mole-rats, hummingbirds and pandas](https://realtech.media/media/2026/11/abb600cad2bbcd2a.jpg)
*Yuliya Elizarova, Wikimedia Commons, CC BY-SA 4.0*

A review in The Innovation Life examines pseudogenes, gene copies inactivated by mutation and long labelled "junk DNA", in vertebrate adaptation and human disease [1]. The authors synthesize recent work on their evolutionary dynamics and functional roles. The human genome alone carries roughly 14,000 pseudogenes [1]. Current identification strategies compare species and screen homologous genes for loss-of-function mutations, which separates genuine gene loss from assembly errors [1].

## Gene loss as adaptation

The review describes a recurring pattern: when a lineage enters a new habitat, genes that once mattered become dispensable, and their inactivation can be adaptive [1]. It assembles cases for immunity, senses, metabolism and diet.

In cetaceans, the bacterial-flagellin receptor TLR5 was pseudogenized. Functional work cited in the review shows that its loss dampens damaging inflammation and improves survival after infection [1]. In the naked mole-rat, underground life relaxed selection on vision: several phototransduction and retinal-integrity genes accumulated inactivating mutations, producing a highly degenerate eye [1].

In hummingbirds, pseudogenization of FBP2, a muscle-specific gluconeogenic enzyme gene, enhances glycolytic flux, mitochondrial biogenesis and respiratory capacity [1]. In the giant panda, loss of DUOX2 coincided with the shift to bamboo, weakening thyroid-hormone synthesis and lowering basal metabolic rate. Loss of the umami receptor T1R1 may have accompanied the same dietary change [1].

## Pseudogenes in human disease

In humans, pseudogenes act mostly through duplicated copies that remain transcribed, via non-coding networks, truncated peptides or cis-regulatory DNA elements [1]. PTENP1, a pseudogene of the tumor suppressor PTEN, sponges microRNAs and lifts repression on PTEN, curbing cancer-cell proliferation [1]. HBBP1 modulates TAL1 and eases beta-thalassemia, while TDGF1P3 transcripts drive tumor progression [1].

The authors note an asymmetry. Pseudogene-derived regulatory RNAs are well documented in disease but untested in adaptive evolution, largely because adaptation research has centered on unitary pseudogenes and non-model species resist functional experiments [1]. They propose long-read RNA sequencing and CRISPR/Cas9 base editing, which can introduce or revert stop codons, as ways to test causal roles [1]. Convergent pseudogenization in distant species under similar pressures is described as a useful model for the predictability of evolutionary trajectories [1].

## Sources

1. [The Innovation Life](https://doi.org/10.59717/j.xinn-life.2026.100240)
2. [EurekAlert](https://www.eurekalert.org/news-releases/1151581)

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Source: RealTech, realtech.media — https://realtech.media/news/rt-bc0cf647c6a6ed02b72b0003_review_gene_inactivation/