Gene Ontology annotation through association of InterPro records with GO terms

Annotation inferences using phylogenetic trees

Combined Automated Annotation using Multiple IEA Methods

Evolution of the vertebrate twist family and synfunctionalization: a mechanism for differential gene loss through merging of expression domains.

Phylogenetic survey of twist genes; the paper cited on the UniProt record but not a sea urchin functional study.

"Twist genes are essential for embryonic development and are conserved from jellyfish to human."

PMID:18495103

Twist is an essential regulator of the skeletogenic gene regulatory network in the sea urchin embryo.

The S. purpuratus twist gene (204 aa; GenBank DAA06084, the source of UniProt A7Z0B7) was identified in silico from the genome; all functional work was done on the L. variegatus orthologue (92% identical).

"we identified the Sptwist gene in silico , which encodes a 204 amino acid polypeptide, by blasting the assembly of S. purpuratus genome with the coding sequence of Lvtwist"
GenBank DAA06084 was deposited by this study.

"Strongylocentrotus purpuratus Twist protein sequence was annotated and deposited on GenBank (Accession Number DAA06084 )."
twist is expressed predominantly in ingressing PMCs at mesenchyme blastula and later in the SMC territory.

"At early mesenchyme blastula (MB) stage, Lvtwist mRNA is predominantly expressed in ingressing PMCs"
Knockdown or overexpression of Twist perturbs successive phases of PMC development.

"Perturbations of Twist either by morpholino knockdown or by overexpression result in defects in progressive phases of PMC development, including specification, ingression/EMT, differentiation and skeletogenesis."
Twist is required for maintenance of the PMC specification state through reciprocal regulation with Alx1.

"Evidence is presented that Twist expression is required for the maintenance of the PMC specification state, and a reciprocal regulation between Alx1 and Twist offers stability for the subsequent processes, such as PMC differentiation and skeletogenesis."
Twist morphants show delayed ingression and no larval skeleton; biomineralization gene transcripts are reduced.

"Downstream of Twist, the mRNA expression level of Lvmsp130, Lvsm50 , and Lvsm30 were examined by QPCR, and were all significantly reduced in Twi morphants when compared to MB controls"
Twist is required cell-autonomously in micromeres for timely ingression, migration and PMC fusion.

"The chimeras show that Twist is essential in micromeres for these cells to ingress punctually and migrate properly into the blastocoel as PMCs."
Whether the Alx1-Twist regulatory inputs are direct was not tested.

"However, whether this mutually positive regulation is due to direct intergenic inputs will requires further examination to confirm the relationship, such as cis-regulatoy analyses."
Secondary mesenchyme derivatives (pigment cells, muscle) are also reduced in morphants.

"Other SMC-associated phenotypes were also observed to persist including reduction of pigment cells ( Fig. 3E,K ; Fig. S1 ) and absence of muscle"

PMID:24598159

Sub-circuits of a gene regulatory network control a developmental epithelial-mesenchymal transition.

twist (with snail) is part of the L. variegatus skeletogenic GRN but not of the published S. purpuratus GRN model.

"The biggest difference between the current S. purpuratus GRN model and that shown in Fig. 1 is the observation that snail and twist are part of the L. variegatus GRN (Wu et al., 2007; Wu et al., 2008 )."
twist is one of 13 PMC transcription factors required for EMT, downstream of alx1/ets1/tbr.

"Three TFs highest in the GRN specified and activated EMT (alx1, ets1, tbr) and the 10 TFs downstream of those (tel, erg, hex, tgif, snail, twist, foxn2/3, dri, foxb, foxo) were also required for EMT."
alx1, twist and snail form a positive-feedback sub-circuit controlling de-adhesion; twist morphant PMCs complete all EMT steps except de-adhesion.

"Therefore, alx1, twist and snail display control over adhesive state change and make a distinct sub-circuit of the GRN, a positive-feedback lockdown, that governs the de-adhesion process ( Fig. 7E )."
Twist positively regulates alx1 in the de-adhesion sub-circuit.

"In the sea urchin de-adhesion sub-circuit, alx1 is upstream of both twist and snail, with twist also positively regulating alx1."

PMID:18413610

Global regulatory logic for specification of an embryonic cell lineage.

The S. purpuratus skeletogenic GRN model lists alx1, ets1, tbr, tel, erg, hex, foxb and dri as drivers of the differentiation genes; twist is not a node of this model.

"these differentiation genes require as drivers products of all of the now familiar components of the skeletogenic regulatory state ( alx1 , ets1 , tbr , tel , erg , hex , foxb , dri )"