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Peer-reviewedCC BYCells

METTL14 Promotes Chicken Preadipocyte Differentiation by Modulating mRNA Stability via a Dual-Reader m⁶A Mechanism.

5 affiliations
  1. 1Key Laboratory of Chicken Genetics and Breeding, Ministry of Agriculture and Rural Affairs, Harbin 150030, China.
  2. 2Key Laboratory of Animal Genetics, Breeding and Reproduction, Education Department of Heilongjiang Province, Harbin 150030, China.
  3. 3College of Animal Science and Technology, Northeast Agricultural University, Harbin 150030, China.
  4. 4Key Laboratory of Exploration and Innovative Utilization of White Goose Germplasm Resources in the Cold Region of Heilongjiang Province, #2 Xinyang Road, New Development District, Daqing 163319, China.
  5. 5College of Animal Science and Technology, Heilongjiang Bayi Agricultural University, #2 Xinyang Road, New Development District, Daqing 163319, China.

Abstract

Preadipocyte differentiation is an essential process in adipogenesis. METTL14, an essential constituent of the N⁶-methyladenosine (m⁶A) methyltransferase complex, plays an important role in mammalian preadipocyte differentiation. However, its role in avian adipogenesis remains unclear. More importantly, the m⁶A mechanism by which METTL14 regulates preadipocyte differentiation has not been elucidated. Here, we found that the level of METTL14 expression was substantially elevated within the adipose tissue of the abdominal region of fat chickens relative to lean chickens. Knockdown of METTL14 inhibited preadipocyte differentiation, whereas overexpression of METTL14 promoted this process. Through the integration of MeRIP-seq and RNA-seq, we confirmed that chBMI1, chTMED3, and chMFAP2 were functionally essential targets of METTL14-dependent m⁶A modification in adipogenesis. METTL14-mediated chBMI1 mRNA stabilization and the degradation of chTMED3 and chMFAP2 mRNAs depend on IGF2BP1/2 and YTHDF2, respectively. Overall, our findings establish that METTL14 promotes chicken preadipocyte differentiation by modulating the stability of target mRNAs through a dual-reader m⁶A mechanism.

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BibTeX
@article{zhang2026mettl14,
  title = {{METTL14 Promotes Chicken Preadipocyte Differentiation by Modulating mRNA Stability via a Dual-Reader m⁶A Mechanism.}},
  author = {Saibo Zhang and Qi Zhang and Yawen Yang and Chang Liu and Fei Teng and Shouzhi Wang and Hui Li and Bohan Cheng},
  journal = {Cells},
  year = {2026},
  month = sep,
  doi = {10.3390/cells15191761},
  url = {https://europepmc.org/article/MED/42882459},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - METTL14 Promotes Chicken Preadipocyte Differentiation by Modulating mRNA Stability via a Dual-Reader m⁶A Mechanism.
AU  - Saibo Zhang
AU  - Qi Zhang
AU  - Yawen Yang
AU  - Chang Liu
AU  - Fei Teng
AU  - Shouzhi Wang
AU  - Hui Li
AU  - Bohan Cheng
PY  - 2026
DA  - 2026/09/27
JO  - Cells
DO  - 10.3390/cells15191761
UR  - https://europepmc.org/article/MED/42882459
AB  - Preadipocyte differentiation is an essential process in adipogenesis. METTL14, an essential constituent of the N⁶-methyladenosine (m⁶A) methyltransferase complex, plays an important role in mammalian preadipocyte differentiation. However, its role in avian adipogenesis remains unclear. More importantly, the m⁶A mechanism by which METTL14 regulates preadipocyte differentiation has not been elucidated. Here, we found that the level of METTL14 expression was substantially elevated within the adipose tissue of the abdominal region of fat chickens relative to lean chickens. Knockdown of METTL14 inhibited preadipocyte differentiation, whereas overexpression of METTL14 promoted this process. Through the integration of MeRIP-seq and RNA-seq, we confirmed that chBMI1, chTMED3, and chMFAP2 were functionally essential targets of METTL14-dependent m⁶A modification in adipogenesis. METTL14-mediated chBMI1 mRNA stabilization and the degradation of chTMED3 and chMFAP2 mRNAs depend on IGF2BP1/2 and YTHDF2, respectively. Overall, our findings establish that METTL14 promotes chicken preadipocyte differentiation by modulating the stability of target mRNAs through a dual-reader m⁶A mechanism.
SN  - 2073-4409
ER  -