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<p>The diverse pigmentation patterns of animals are crucial for predation avoidance and behavioral display. This diversity arises from interactions among distinct pigment cell types, yet mechanisms generating pattern variation across teleost fishes remain incompletely understood. In zebrafish, Turing models have been proposed to explain stripe patterns, but it is unclear if they apply to other fishes. Here, we investigate the <i>Snowflake</i> mutant of the anemonefish <i>Amphiprion ocellaris</i>, which displays enlarged white bars with irregular boundaries. Using genome-wide association mapping and targeted sequencing, we identify a missense mutation (E42K) in <i>gja5b</i>, encoding the gap junction protein Connexin 41.8. CRISPR/Cas9-mediated genome editing recapitulates the <i>Snowflake</i> phenotype, while pharmacological inhibition of gap junctions phenocopies the boundary defects, supporting a causal role for impaired intercellular communication. Expression analyses reveal that, unlike zebrafish, anemonefish <i>gja5b</i> is predominantly expressed in iridophores. With functional in vitro assays we demonstrate that the E42K mutation acts as a dominant negative, strongly reducing gap junctional coupling. Introducing the same mutation in zebrafish reveals context-dependent effects on pigment patterning. Taken together our findings highlighting gap junction–mediated communication as a conserved but flexible mechanism controlling pigment boundary positioning and pattern diversification.</p>

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Cell-cell communication as underlying principle governing color pattern formation in teleost fishes

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年2月18日

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  • Marleen Klann,
  • Saori Miura,
  • Shu-Hua Lee,
  • Stefano Davide Vianello,
  • Robert Ross,
  • Masakatsu Watanabe,
  • Emma Gairin,
  • Yipeng Liang,
  • Harrison W. Hutto,
  • Braedan M. McCluskey,
  • Marcela Herrera,
  • Lila Solnica-Krezel,
  • Laurence Besseau,
  • Simone Pigolotti,
  • David M. Parichy,
  • Masato Kinoshita,
  • Vincent Laudet

摘要

The diverse pigmentation patterns of animals are crucial for predation avoidance and behavioral display. This diversity arises from interactions among distinct pigment cell types, yet mechanisms generating pattern variation across teleost fishes remain incompletely understood. In zebrafish, Turing models have been proposed to explain stripe patterns, but it is unclear if they apply to other fishes. Here, we investigate the Snowflake mutant of the anemonefish Amphiprion ocellaris, which displays enlarged white bars with irregular boundaries. Using genome-wide association mapping and targeted sequencing, we identify a missense mutation (E42K) in gja5b, encoding the gap junction protein Connexin 41.8. CRISPR/Cas9-mediated genome editing recapitulates the Snowflake phenotype, while pharmacological inhibition of gap junctions phenocopies the boundary defects, supporting a causal role for impaired intercellular communication. Expression analyses reveal that, unlike zebrafish, anemonefish gja5b is predominantly expressed in iridophores. With functional in vitro assays we demonstrate that the E42K mutation acts as a dominant negative, strongly reducing gap junctional coupling. Introducing the same mutation in zebrafish reveals context-dependent effects on pigment patterning. Taken together our findings highlighting gap junction–mediated communication as a conserved but flexible mechanism controlling pigment boundary positioning and pattern diversification.