Skeletal Malformations Induced by Mitomycin C in Chick Embryos

Singh, Jasmeet; Singh, Simranjeet

doi:10.3109/17453677608988729

Cited by 3 publications

(2 citation statements)

References 8 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The twisted bone phenotype is most likely not due to defects in patterning the early limb, because the twisting occurs after condensation of the primordia of the skeletal elements. This class of skeletal defect has been previously seen in limb buds displaying a reduction in size, e.g., due to Goosecoid misexpression in chicks (28) and in compound mutations in Prx1 and Prx2 mice (29).This phenotype can, in fact, be mimicked by the blocking of cell proliferation in chick limb buds (32), indicating that a decrease in the size of the limb primordia is sufficient to lead to the twisting of the skeletal elements.…”

Section: Discussionmentioning

confidence: 53%

The RNaseIII enzyme Dicer is required for morphogenesis but not patterning of the vertebrate limb

Harfe

McManus

Mansfield

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

622

648

View full text Add to dashboard Cite

The RNaseIII-containing enzyme Dicer is believed to be required for the processing of most, if not all, microRNAs (miRNAs) and for processing long dsRNA into small interfering RNAs. Because the complete loss of Dicer in both zebrafish and mice results in early embryonic lethality, it has been impossible to determine what role, if any, Dicer has in patterning later tissues in the developing vertebrate embryo. To bypass the early requirement of Dicer in development, we have created a conditional allele of this gene in mice. Using transgenes to drive Cre expression in discrete regions of the limb mesoderm, we find that removal of Dicer results in the loss of processed miRNAs. Phenotypically, developmental delays, in part due to massive cell death as well as disregulation of specific gene expression, lead to the formation of a much smaller limb. Thus, Dicer is required for the formation of normal mouse limbs. Strikingly, however, we did not detect defects in basic patterning or in tissue-specific differentiation of Dicer-deficient limb buds.microRNAs ͉ mouse

show abstract

Section: Discussionmentioning

confidence: 53%

The RNaseIII enzyme Dicer is required for morphogenesis but not patterning of the vertebrate limb

Harfe

McManus

Mansfield

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

622

648

View full text Add to dashboard Cite

show abstract

“…This observation suggests that the developing limb is plastic yet has a developmental bias favored towards its proximo-distal (shoulder to fingertip) segmentation. Evidence supporting this idea has been observed across a range of experimental models that induce limb progenitor cell (LPC) cell cycle defects and/or cell death [3][4][5][6][7][8] , including Wolpert's classical X-irradiation experiment 9 that was mechanistically resolved much later 10 . However, an integrated understanding of limb plasticity at the molecular and cellular level upon changes in LPC number remains unclear.…”

Section: Introductionmentioning

confidence: 97%

Integrated multi-omics reveals minor spliceosome inhibition causes molecular stalling and developmental delay of the mouse forelimb

Drake

Springer

Afriyie

et al. 2022

Preprint

View full text Add to dashboard Cite

Developmental insults causing limb progenitor cell cycle defects or death tend to produce micromelic limbs with maintained segmentation. This suggests that the developing limb is plastic yet has a bias towards proximo-distal patterning. Here we use a minor spliceosome-deficient (U11-null) mouse forelimb, which has severe micromelia yet maintains proximo-distal segmentation, to decipher the mechanism(s) underlying this form of developmental robustness. We show that U11 loss triggers transcriptomic stalling upon spatially heterogenous mis-splicing of minor intron-containing genes. Through spatial transcriptomics, we detected a failure of the U11-null forelimb to separate its distal patterning program from its proximal differentiation program, which was supported by single-cell RNAseq-determined developmental delay of U11-null chondroprogenitors. Ultimately, these molecular and cellular deficits culminated in perturbed chondrogenesis, myogenesis, and axonogenesis. Taken together, we suggest that, upon sensing depletion of progenitors, the limb halts its transcriptional networks to pause its cellular trajectory, affording time to restructure its developmental program.

show abstract

Toxicity and Teratogenic Effects of Zinc Sulfide Nanoparticles on Chick Embryo and Chick Fibroblast Cell Culture

Asadi

Abdolmaleki

2019

Horizon Med Sci

View full text Add to dashboard Cite

Aims Nanoparticles (particles with a diameter of 10-500 nm) are currently used in the cosmetics industry as well as for pharmaceuticals, diagnostic imaging, and tissue engineering. Since these nanoparticles are used in industry and drug delivery, they can also be used by pregnant women. Thus, the current study investigated the teratogenic and cytotoxic effects of Zinc Sulfide (ZnS) nanoparticles on the embryo and their fibroblastic cell culture. Methods & Materials Zinc sulfide (ZnS) nanoparticles were synthesized. Then, nanoparticles at the concentrations of 5, 10, 15, 30, and 40 mg/mL/egg were injected into the air sac of the eggs in three replicates on the third day of incubation. Next, the treated and control eggs, on day 19 of incubation were opened, and embryos were weighted, and the relevant mortality rate was recorded. Fibroblast cells were isolated, cultured, and treated from the control embryo, and morphological changes and cell survival percentages were recorded. Findings The obtained results revealed that the embryos’ survival rate depends on the nanoparticle concentration. As a result, at the highest concentration, only 36.32% of the embryos survived, and the lethal dose 50% (LD50) was equal to 32.47 mg/egg. Morphological study of the treated embryos club foot and skeletal staining suggested the deletion of caudal vertebrate. The cytotoxicity study results of ZnS nanoparticles on fibroblastic cells indicated the survival fractions of 88.45%, 68.75%, and 49.32%, respectively, and its IC50 value was measured aas1460 μM. Conclusion The present study results suggested that ZnS nanoparticles had no significant toxic effects on the embryos and culture of chicken fibroblastic cells at low concentrations.

show abstract

Skeletal Malformations Induced by Mitomycin C in Chick Embryos

Cited by 3 publications

References 8 publications

The RNaseIII enzyme Dicer is required for morphogenesis but not patterning of the vertebrate limb

The RNaseIII enzyme Dicer is required for morphogenesis but not patterning of the vertebrate limb

Integrated multi-omics reveals minor spliceosome inhibition causes molecular stalling and developmental delay of the mouse forelimb

Toxicity and Teratogenic Effects of Zinc Sulfide Nanoparticles on Chick Embryo and Chick Fibroblast Cell Culture

Contact Info

Product

Resources

About