Transcriptional Profiles of Skeletal Muscle Associated With Increasing Severity of White Striping in Commercial Broilers
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DOI:
10.3389/fphys.2020.00580
Publication Date:
2020-06-16T04:19:45Z
AUTHORS (9)
ABSTRACT
Development of the white striping (WS) abnormality adversely impacts overall quality broiler breast meat. Its etiology remained unclear. This study aimed at exploring transcriptional profiles skeletal muscles exhibiting different WS severity to elucidate molecular mechanisms underlying development and progression WS. Total RNA was isolated from pectoralis major male 7-week-old Ross 308 broilers. The samples were classified as mild (n = 6), moderate 6) or severe 4), based on number thickness striations meat surface. transcriptome profiled using a chicken gene expression microarray with one-color hybridization technique. Gene patterns each level compared against other; hence, there three comparisons: vs. (C1), (C2), (C3). Differentially expressed genes (DEGs) identified combined criteria false discovery rate 0.2 absolute fold change 1.2. Differential 91, 136 294 transcripts in C1, C2 C3, respectively. There no DEGs common among comparisons. Based pathway analysis, enriched pathways C1 related impaired homeostasis macronutrients small biochemical molecules disrupted Ca2+-related pathways. Decreased abundance period circadian regulator suggested shifted phase when developed. uniquely obtained degradation, Ras signaling, cellular senescence, axon guidance salivary secretion. those might play crucial roles regulating ion balances cell-cycle arrest. In responsible for phosphatidylinositol 3-kinase-Akt p53 activation, apoptosis hypoxia-induced processes modified. Additionally, associated variety diseases involved regulation [Ca2+], collagen formation, microtubule-based motor, immune response identified. Eight all comparisons (i.e. calcium Ras-associated protein 1 ubiquitination-mediated proteolysis, vascular smooth muscle contraction, oxytocin signaling cancer). current findings support role intracellular imbalance, particularly Ca2+, oxidative stress, programmed cell death progression.
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