Molecular motor MYO1C, acetyltransferase KAT6B and osteogenetic transcription factor RUNX2 expression in human masseter muscle contributes to development of malocclusion.
OBJECTIVE
Type I myosins are molecular motors necessary for glucose transport in the cytoplasm and initiation of transcription in the nucleus. Two of these, MYO1H and MYO1C, are paralogs which may be important in the development of malocclusion. The objective of this study was to investigate their gene expression in the masseter muscle of malocclusion subjects. Two functionally related proteins known to contribute to malocclusion were also investigated: KAT6B (a chromatin remodelling epigenetic enzyme which is activated by MYO1C) and RUNX2 (a transcription factor regulating osteogenesis which is activated by KAT6B).


METHODS
Masseter muscle samples and malocclusion classifications were obtained from orthognathic surgery subjects. Muscle was sectioned and immunostained to determine fibre type properties. RNA was isolated from the remaining sample to determine expression levels for the four genes by TaqMan(®) RT-PCR. Fibre type properties, gene expression quantities and malocclusion classification were compared.


RESULTS
There were very significant associations (P<0.0000001) between MYO1C and KAT6B expressions. There were also significant associations (P<0.005) between RUNX2 expression and masseter muscle type II fibre properties. Very few significant associations were identified between MYO1C and masseter muscle fibre type properties.


CONCLUSIONS
The relationship between MYO1C and KAT6B suggests that the two are interacting in chromatin remodelling for gene expression. This is the nuclear myosin1 (NM1) function of MYO1C. A surprising finding is the relationship between RUNX2 and type II masseter muscle fibres, since RUNX2 expression in mature muscle was previously unknown. Further investigations are necessary to elucidate the role of RUNX2 in adult masseter muscle.
Orthodontic Private Practice,1649 Bluebird Canyon Drive, Laguna Beach, CA, United States.
Heather
H
Desh
Orthodontic Department, Temple University, 3223 North Broad Street, Philadelphia, PA, United States.
S Lauren
SL
Gray
Orthodontic Department, Temple University, 3223 North Broad Street, Philadelphia, PA, United States.
Michael J
MJ
Horton
Oral and Maxillofacial Surgery, Université Lille Nord de France, UDSL, Roger Salengro Hospital, CHU, and INSERM U 1008, Controlled Drug Delivery Systems and Biomaterials, Lille, France.
Gwenael
G
Raoul
Centre of Human and Aerospace Physiological Sciences, King's College London, London, UK.
Anthea M
AM
Rowlerson
Oral and Maxillofacial Surgery, Université Lille Nord de France, UDSL, Roger Salengro Hospital, CHU, and INSERM U 1008, Controlled Drug Delivery Systems and Biomaterials, Lille, France.
Joel
J
Ferri
Department of Oral Biology, School of Dental Medicine, University of Pittsburgh, 3501 Terrace Street, Pittsburgh, PA, United States.
Alexandre R
AR
Vieira
Orthodontic Department, Temple University, 3223 North Broad Street, Philadelphia, PA, United States. Electronic address: jjs6@dental.temple.edu.
James J
JJ
Sciote
D050659:Core Binding Factor Alpha 1 Subunit / Q000235:genetics*; D005260:Female; D015870:Gene Expression; D051548:Histone Acetyltransferases / Q000235:genetics*; D006801:Humans; D008297:Male; D008310:Malocclusion / Q000145:classification / Q000235:genetics*; D008406:Masseter Muscle / Q000378:metabolism*; D024461:Myosin Type I / Q000235:genetics*; D060888:Real-Time Polymerase Chain Reaction; D055815:Young Adult
D050659:Core Binding Factor Alpha 1 Subunit; C493709:RUNX2 protein, human; D051548:Histone Acetyltransferases; C487137:KAT6B protein, human; D024461:Myosin Type I; C460367:MYO1C protein, human
KAT6B; MYO1C; Malocclusion; Masseter muscle; RUNX2