TY - JOUR

T1 - Cartilaginous fishes offer unique insights into the evolution of the nuclear receptor gene repertoire in gnathostomes

AU - Fonseca, Elza

AU - Machado, Andre M.

AU - Vilas-Arrondo, Nair

AU - Gomes-dos-Santos, Andre

AU - Verissimo, Ana

AU - Esteves, Pedro

AU - Almeida, Tereza

AU - Themudo, Goncalo

AU - Ruivo, Raquel

AU - Perez, Montse

AU - da Fonseca, Rute

AU - Santos, Miguel M.

AU - Froufe, Elsa

AU - Roman-Marcote, Esther

AU - Venkatesh, Byrappa

AU - Castro, L. Filipe C.

PY - 2020

Y1 - 2020

N2 - Nuclear receptors (NRs) are key transcription factors that originated in the common ancestor of metazoans. The vast majority of NRs are triggered by binding to either endogenous (e.g. retinoic acid) or exogenous (e.g. xenobiotics) ligands, and their evolution and expansion is tightly linked to the function of endocrine systems. Importantly, they represent classic targets of physiological exploitation by endocrine disrupting chemicals. The NR gene repertoire in different lineages has been shaped by gene loss, duplication and mutation, denoting a dynamic evolutionary route. As the earliest diverging class of gnathostomes (jawed vertebrates), cartilaginous fishes offer an exceptional opportunity to address the early diversification of NR gene families and the evolution of the endocrine system in jawed vertebrates. Here we provide an exhaustive analysis into the NR gene composition in five elasmobranch (sharks and rays) and two holocephalan (chimaeras) species. For this purpose, we generated also a low coverage draft genome assembly of the chimaera small-eyed rabbitfish, Hydrolagus affinis. We show that cartilaginous fish retain an archetypal NR gene repertoire, similar to that of mammals and coincident with the two rounds of whole genome duplication that occurred in the gnathostome ancestor. Furthermore, novel gene members of the non-canonical NR0B receptors were found in the genomes of this lineage. Our findings provide an essential view into the early diversification of NRs in gnathostomes, paving the way for functional studies.

AB - Nuclear receptors (NRs) are key transcription factors that originated in the common ancestor of metazoans. The vast majority of NRs are triggered by binding to either endogenous (e.g. retinoic acid) or exogenous (e.g. xenobiotics) ligands, and their evolution and expansion is tightly linked to the function of endocrine systems. Importantly, they represent classic targets of physiological exploitation by endocrine disrupting chemicals. The NR gene repertoire in different lineages has been shaped by gene loss, duplication and mutation, denoting a dynamic evolutionary route. As the earliest diverging class of gnathostomes (jawed vertebrates), cartilaginous fishes offer an exceptional opportunity to address the early diversification of NR gene families and the evolution of the endocrine system in jawed vertebrates. Here we provide an exhaustive analysis into the NR gene composition in five elasmobranch (sharks and rays) and two holocephalan (chimaeras) species. For this purpose, we generated also a low coverage draft genome assembly of the chimaera small-eyed rabbitfish, Hydrolagus affinis. We show that cartilaginous fish retain an archetypal NR gene repertoire, similar to that of mammals and coincident with the two rounds of whole genome duplication that occurred in the gnathostome ancestor. Furthermore, novel gene members of the non-canonical NR0B receptors were found in the genomes of this lineage. Our findings provide an essential view into the early diversification of NRs in gnathostomes, paving the way for functional studies.

KW - Nuclear receptors

KW - Genome

KW - Gene loss

KW - Gene duplication

KW - HORMONE-RECEPTORS

KW - GENOME

KW - CHONDRICHTHYES

KW - TRANSCRIPTION

KW - EXPLOITATION

KW - SPECIFICITY

KW - AMPHIOXUS

KW - QUALITY

KW - SHARK

KW - RXR

U2 - 10.1016/j.ygcen.2020.113527

DO - 10.1016/j.ygcen.2020.113527

M3 - Journal article

C2 - 32526329

VL - 295

JO - General and Comparative Endocrinology

JF - General and Comparative Endocrinology

SN - 0016-6480

M1 - 113527

ER -