SynthesisFrontiers in pharmacology2022
The evolutionary conservation of eukaryotic membrane-bound adenylyl cyclase isoforms.
Synthesis in Frontiers in pharmacology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 12 citations in OpenAlex.
- Origins and Molecular Features of a Chimeric Type-P4A ATPase-Guanylate Cyclase from Stramenopiles and Alveolates.International journal of molecular sciences · 2026Article
- Lipid regulation of adenylyl cyclase Rv1625c from Mycobacterium tuberculosis by its membrane-domain receptor.The FEBS journal · 2025Article
- A signal transduction blind spot: the function of adenylyl cyclase transmembrane domains.The FEBS journal · 2025Review
- Article
- Contribution of membrane-associated oscillators to biological timing at different timescales.Frontiers in physiology · 2023Article
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1 author at 1 institution in 1 country.
Funding
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Abstract
The nine membrane-delimited eukaryotic adenylyl cyclases are pseudoheterodimers with an identical domain order of seven (nine) distinct subdomains. Bioinformatics show that the protein evolved from a monomeric bacterial progenitor by gene duplication and fusion probably in a primordial eukaryotic cell around 1.5 billion years ago. Over a timespan of about 1 billion years, the first fusion product diverged into nine highly distinct pseudoheterodimeric isoforms. The evolutionary diversification ended approximately 0.5 billion years ago because the present isoforms are found in the living fossil coelacanth, a fish. Except for the two catalytic domains, C1 and C2, the mAC isoforms are fully diverged. Yet, within each isoform a high extent of conservation of respective subdomains is found. This applies to the C- and N-termini, a long linker region between the protein halves (C1b), two short cyclase-transducing-elements (CTE) and notably to the two hexahelical membrane domains TM1 and TM2. Except for the membrane anchor all subdomains were previously implicated in regulatory modalities. The bioinformatic results unequivocally indicate that the membrane anchors must possess an important regulatory function specifically tailored for each mAC isoform.
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