MSTN mutant promoted bovine muscle satellite cell proliferation by regulating the binding of SMAD2/SMAD3 with CDKN1C

Gao, Li; Yang, Miaomiao; Gu, Mingjuan; Liu, Yunpeng; Bu, Cai-Hong; Cheng, Peng; Bai, Chunling

doi:10.21203/rs.3.rs-620883/v1

Cited by 2 publications

(4 citation statements)

References 24 publications

(43 reference statements)

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“…24 It was also shown that MSTN deficiency promotes bovine muscle satellite cell proliferation by regulating the binding of SMAD2/ SMAD3 with CDKN1C. 25 Briefly, MSTN deficiency downregulated the expression of SMAD2/SMAD3, reduced the promotion of SMAD2/SMAD3 to the CDKN1C expression, inhibited the CDKN1C expression, elevated cell cycle-related gene expression (CyclinA-CDK2), leading to the promotion of cell proliferation. 25 TALENs were also applied to target the bovine MSTN gene, 26−29 and live TALENs-mediated MSTN knockout cattle were generated using ovum pickup, in vitro fertilization, and zygote microinjection (OPU-IVF-ZM) 29 (Table 1).…”

Section: ■ Targeting the Mstn Gene In Cattlementioning

confidence: 99%

“…25 Briefly, MSTN deficiency downregulated the expression of SMAD2/SMAD3, reduced the promotion of SMAD2/SMAD3 to the CDKN1C expression, inhibited the CDKN1C expression, elevated cell cycle-related gene expression (CyclinA-CDK2), leading to the promotion of cell proliferation. 25 TALENs were also applied to target the bovine MSTN gene, 26−29 and live TALENs-mediated MSTN knockout cattle were generated using ovum pickup, in vitro fertilization, and zygote microinjection (OPU-IVF-ZM) 29 (Table 1). More recently, CRISPR/Cas9 was applied to edit the bovine MSTN gene in vitro 30−32 and in vivo 33−35 (Table 1).…”

Section: ■ Targeting the Mstn Gene In Cattlementioning

confidence: 99%

“…The inferred mechanism is that the MSTN deficiency inhibited SMAD2/SMAD3, activated TET1 , and increased myogenesis-specific gene expression ( PAX3 , PAX7 , MyoD , MyoG , and MYF5 ), leading to an induction of myogenic differentiation . It was also shown that MSTN deficiency promotes bovine muscle satellite cell proliferation by regulating the binding of SMAD2/SMAD3 with CDKN1C . Briefly, MSTN deficiency downregulated the expression of SMAD2/SMAD3, reduced the promotion of SMAD2/SMAD3 to the CDKN1C expression, inhibited the CDKN1C expression, elevated cell cycle-related gene expression ( CyclinA - CDK2 ), leading to the promotion of cell proliferation …”

Section: Targeting the Mstn Gene In Cattlementioning

confidence: 99%

“…It was also shown that MSTN deficiency promotes bovine muscle satellite cell proliferation by regulating the binding of SMAD2/SMAD3 with CDKN1C . Briefly, MSTN deficiency downregulated the expression of SMAD2/SMAD3, reduced the promotion of SMAD2/SMAD3 to the CDKN1C expression, inhibited the CDKN1C expression, elevated cell cycle-related gene expression ( CyclinA - CDK2 ), leading to the promotion of cell proliferation …”

Section: Targeting the Mstn Gene In Cattlementioning

confidence: 99%

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When Less Is More: Targeting the Myostatin Gene in Livestock for Augmenting Meat Production

Kalds

Zhou

Huang

et al. 2023

J. Agric. Food Chem.

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How to increase meat production is one of the main questions in animal breeding. Selection for improved body weight has been made and, due to recent genomic advances, naturally occurring variants that are responsible for controlling economically relevant phenotypes have been revealed. The myostatin (MSTN) gene, a superstar gene in animal breeding, was discovered as a negative controller of muscle mass. In some livestock species, natural mutations in the MSTN gene could generate the agriculturally desirable double-muscling phenotype. However, some other livestock species or breeds lack these desirable variants. Genetic modification, particularly gene editing, offers an unprecedented opportunity to induce or mimic naturally occurring mutations in livestock genomes. To date, various MSTN-edited livestock species have been generated using different gene modification tools. These MSTN gene-edited models have higher growth rates and increased muscle mass, suggesting the high potential of utilizing MSTN gene editing in animal breeding. Additionally, post-editing investigations in most livestock species support the favorable influence of targeting the MSTN gene on meat quantity and quality. In this Review, we provide a collective discussion on targeting the MSTN gene in livestock to further encourage its utilization opportunities. It is expected that, shortly, MSTN gene-edited livestock will be commercialized, and MSTN-edited meat will be on the tables of ordinary customers.

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