No abstract

Across the animal kingdom, lizards are the only amniotes capable of regenerating their lost tail through epimorphosis. Of the many reptiles, the northern house gecko, Hemidactylus flaviviridis, is an excellent model system that is used for understanding the mechanism of epimorphic regeneration. A stage-specific transcriptome profile was generated in the current study following an autotomized tail with the HiSeq2500 platform. The reads obtained from de novo sequencing were filtered and high-quality reads were considered for gene ontology (GO) annotation and pathway analysis. Millions of reads were recorded for each stage upon de novo assembly. Up and down-regulated transcripts were categorized for early blastema (EBL), blastema (BL) and differentiation (DF) stages compared to the normal tail (NT) by differential gene expression analysis. The transcripts from developmentally significant pathways such as FGF, Wnt, Shh and TGF-β/BMP were present during tail regeneration. Additionally, differential expression of transcripts was recorded from biological processes, namely inflammation, cell proliferation, apoptosis and cell migration. Overall, the study reveals the stage-wise transcriptome analysis in conjunction with cellular processes as well as molecular signaling pathways during lizard tail regeneration. The knowledge obtained from the data can be extrapolated to configure regenerative responses in other amniotes, including humans, upon loss of a complex organ.

No abstract

A recent study from our lab revealed that the inhibition of cyclooxygenase-2 (COX-2) exclusively reduces the level of PGE2 (Prostaglandin E2) among prostanoids and hampers the normal development of several structures, strikingly the cranial vault, in chick embryos. In order to unearth the mechanism behind the deviant development of cranial features, the expression pattern of various factors that are known to influence cranial neural crest cell (CNCC) migration was checked in chick embryos after inhibiting COX-2 activity using etoricoxib. The compromised level of cell adhesion molecules and their upstream regulators, namely CDH1 (E-cadherin), CDH2 (N-cadherin), MSX1 (Msh homeobox 1), and TGF-β (Transforming growth factor beta), observed in the etoricoxib-treated embryos indicate that COX-2, through its downstream effector PGE2, regulates the expression of these factors perhaps to aid the migration of CNCCs. The histological features and levels of FoxD3 (Forkhead box D3), as well as PCNA (Proliferating cell nuclear antigen), further consolidate the role of COX-2 in the migration and survival of CNCCs in developing embryos. The results of the current study indicate that COX-2 plays a pivotal role in orchestrating craniofacial structures perhaps by modulating CNCC proliferation and migration during the embryonic development of chicks.

Oesophageal disorders are relatively uncommon in large animals. Oesophageal obstruction is the most frequently encountered clinical presentation in bovine and it may be intraluminal or extra luminal (Haven, 1990). Intraluminal obstruction or “choke” is the most common abnormality that usually occurs when foreign objects, large feedstuff, medicated boluses, trichobezoars, or oesophageal granuloma lodge in the lumen of the oesophagus. Oesophageal obstructions in bovine commonly occur at the pharynx, the cranial aspect of the cervical oesophagus, the thoracic inlet, or the base of the heart (Choudhary et al., 2010). Diagnosis of such problem depends on the history of eating particular foodstuff and clinical signs as bloat, tenesmus, retching, and salivation

No abstract

Exposure to chlorpyrifos‐cypermethrin combination during early development resulted in defective looping and ventricular noncompaction of heart in domestic chicken. The study was extended to elucidate the molecular basis of this novel observation. The primary culture of chicken embryonic heart cells showed a concentration‐dependent loss of viability when challenged with this combination of technical‐grade insecticides. Comet assay, DNA ladder assay, and analyses of appropriate markers at transcript and protein levels, revealed that chlorpyrifos‐cypermethrin combination induced cell death by activating apoptosis. Parallelly, the tissues derived from control and experimental group hearts were checked for apoptotic markers, and the result was much similar to that of the in‐vitro study. Further analysis showed that chlorpyrifos‐cypermethrin combination deranged the expression pattern of the transcriptional regulators of cardiogenesis, namely TBX20, GATA5, HAND2, and MYOCD. This, together with heightened apoptosis, could well be the reason behind the observed structural anomalies in the heart of chlorpyrifos‐cypermethrin poisoned embryos.

A recent study from our lab revealed that inhibition of cyclooxygenase-2 exclusively reduces the level of PGE2 amongst the prostanoids and hamper the normal development of several structures, strikingly the cranial vault, in chick embryos. In order to unearth the mechanism behind the deviant development of cranial features, the expression pattern of various factors that are known to influence the cranial neural crest cell (CNCC) migration were checked in chick embryo after inhibiting the COX-2 activity using etoricoxib. The compromised level of cell adhesion molecules and their upstream regulators, namely CDH1, CDH2, MSX1, and TGF-β, observed in the etoricoxib treated embryos indicate that COX-2, through its downstream effector PGE2, regulates the expression of these factors perhaps to aid the migration of CNCC. The histological features and levels of FoxD3 as well as PCNA further consolidates the role of COX-2 in migration and survival of CNCC in developing embryo. The results of the current study indicate that the COX-2 plays a pivotal role in orchestrating the proliferation and migration of CNCC during embryonic development of chick.