Karyotype analysis of the acute fibrosarcoma from chickens infected with subgroup J avian leukosis virus associated with v-srconcogene

Abstract

To understand the cytogenetic characteristics of acute fibrosarcoma in chickens infected with the subgroup J avian leukosis virus associated with the v-src oncogene, we performed a karyotype analysis of fibrosarcoma cell cultures. Twenty-nine of 50 qualified cell culture spreads demonstrated polyploidy of some macrochromosomes, 21 of which were trisomic for chromosome 7, and others were trisomic for chromosomes 3, 4, 5 (sex chromosome w), and 10. In addition, one of them was trisomic for both chromosome 7 and the sex chromosome 5 (w). In contrast, no aneuploidy was found for 10 macrochromosomes of 12 spreads of normal chicken embryo fibroblast cells, although aneuploidy for some microchromosomes was demonstrated in five of the 12 spreads. The cytogenetic mosaicism or polymorphism of the aneuploidy in the acute fibrosarcoma described in this study suggests that the analysed cells are polyclonal. ARTICLE HISTORY

Retracted: MicroRNA‐30d preserves pancreatic islet β‐cell function through negative regulation of the JNK signaling pathway via SOCS3 in mice with streptozotocin‐induced diabetes mellitus

“…Additionally, miR-30d has been reported to play a vital role in influencing the functions of β-cells that are impaired via proinflammatory cytokines and in the activation of glucose-induced insulin gene transcription, which serves as an important target for diabetes intervention (Han, Cao, Wang, Dong, & Chen, 2016). The suppressors of cytokine signaling (SOCS) protein family consist of SOCS1-7 as well as eight other members including cytokine-induced STAT inhibitor (CIS) (Dong et al, 2016), operates as a negative regulatory factor that mainly inhibits the differentiation, proliferation, and induction of apoptosis by suppressing the the Janus kinase (JAK)signal transducer and activator of transcription (STAT) signaling pathway (Liu, Li, Dong, et al, 2016). Therefore, the function of SOCS3 gene may potentially be activated by the antiviral signaling pathway (Aslam et al, 2016).…”

Hi-C analysis of genomic contacts revealed karyotype abnormalities in chicken HD3 cell line

“…However, these data in continuous chicken cell lines are fragmentary and generally limited to the analysis of numerical karyotype abnormalities, such as chromosomal aneuploidies, by classical cytogenetic approaches using Giemsa-stained metaphase spread chromosome preparations and FISH with chromosome-specific probes. Significant deviations from diploid chromosome number have been demonstrated for the hepatocellular carcinoma cell line LMH [ 64 ], avian leukosis cell line LSCC–H32 and CEC-32 cell line [ 65 ], several cell lines derived from Marek’s disease T-cell lymphomas, such as HPRS Line 1 and HPRS Line 2 [ 66 ], ALV-J-induced fibrosarcoma cell line [ 67 ] and others. In many tumor-derived cell lines, chromosomal heteromorphism involving one or several pairs of macrochromosomes has been demonstrated, including amplification of the short arm of chromosome 1 (1p +) in different cell lines from Marek’s disease lymphomas [ 68 ], the heteromorphic chromosome 1 pair in MSB-1, marker chromosomes derived from rearrangements involving chromosome 3 or chromosome 5 and unidentified elements in HPRS Lines 1 and 2 [ 66 ].…”

Regulatory effects of chicken TRIM25 on the replication of ALV-A and the MDA5-mediated type I interferon response

“…ALV is divided into 11 subgroups from A to K according to the host range, antibody neutralization and receptor interference studies, and seven of these subgroups, namely, ALV-A/ B/C/D/E/J/K, can infect chickens [24][25][26][27]. Except for the ALV-E subgroup, the other six subgroups are exogenous ALVs, which can cause severe pathogenicity in chickens [28][29][30]. ALV-E can interfere with the detection of exogenous ALVs because its gene was inserted into the chicken genome early in its evolution, but its pathogenicity is weak [24,31].…”