Cs and Theca cells (TCs) of ovarian follicles and regulated the levels of cAMP and steroid production by way of activation of ADRB2/cAMP/protein kinase A (PKA) signaling pathway and/or ADRB2/ cAMP/protein, phospholipase C (PLC)/protein kinase C (PKC)/cAMP response element-binding protein (CREB) signaling cascade [402]. Nevertheless, the excessive ovarian steroidal response to gonadotropins and beta-adrenergic stimulation enhanced polycystic ovary syndrome (PCOS), an endocrine disorder characterizedSun et al. BMC Genomics(2021) 22:Web page 9 ofFig. four Scatter plot of annotated differently expressed genes and enriched signaling pathways in LYF follicles between JB and LB chickens. A MA plot of differently expressed genes in GWF follicles in between JB and LB samples. JB3, LYF follicle samples of JB hens; LB3, LYF samples of LB hens. B Bubble chart of major 20 of KEGG pathway enrichmentby anovulation, hyperandrogenism and polycystic ovaries [36, 37, 43, 44]. The a great deal abundant expression levels of ADRB2 gene may well induce layer broodiness by activation of adenylate cyclase via the action of G proteins and stimulate anovulation [37, 43]. The hydroxysteroid (17beta) S1PR4 Gene ID dehydrogenase form 1 (HSD17B1) is actually a steroidogenic enzyme encoded by HSD17B1 gene, to effectively catalyze reversible interconversion of a low-active precursor estrogen estrone (E1) for the very active E2 that may be needed for typical ovary PLK2 Purity & Documentation development [13, 45]. It is actually the important isozyme inside the granulosa cells of the ovary and has a central function in regulating the circulating estradiol concentration at the same time as its nearby production in estrogen target cells, locally promotes improvement, differentiation, and maturation in the follicle [468]. Nonetheless, inhibition of HSD17B1 impairs the synthesis of 17-estradiol, and attenuates action with the estradiol [47, 49], which can directly block ovarian follicle development. Moreover, HSD17B1 plays a critical part in controlling cell proliferation and inside the regulation from the development and function of organs [50]. It was recommended that the reduce expression levels of HSD17B1 transcript in SYF follicles of JB hens may well have an effect on ovarian dominant follicle selection and follicle growth and function by repressing 17-estradiol production and follicle cell proliferation, and finally lead to a low egg production. Transcriptomic analysis of LYF follicles revealed higher mRNA levels of CYP2D6, CRH, GABRA1, and GHRHRLR, and decrease mRNA levels of ID4, SSTR2, CDKN1Aand NDUFAB1 genes inside the JB than inside the LB layers. Amongst them, by far the most representative gene GHRHRLR, also named VIPR1, its encoding solution VIPR1 was mainly expressed in granulosa cells and residual ovarian tissue [51]. PACAP might promote oocyte maturation in the maturation phase through VPAC1-R around the follicle cells, whose expression surges in full-grown follicles before maturation and is consistently high in the follicles undergoing final maturation [35]. Furthermore, the genetic polymorphisms of VIP and VIPR1 genes were associated with chicken broodiness and egg production [52, 53]. It was intimated that the greater expression levels of VIPR1 transcript in LYF follicles of JB hens may possibly inhibit ovarian follicle development, differentiation and maturation, and contribute to the lower egg production. Interestingly, the substantially up-regulated GABRA1 mRNA and down-regulated NDUFAB1 mRNA from the GWF, SYF and LYF follicles have been co-expressed differentially in JB hen ovaries when compared with LB hen. Earlier studies have reported t