Sugar signals pedal the cell cycle!

Cell cycle involves the sequential and reiterative progression of important events leading to cell division. Progression through a specific phase of the cell cycle is under the control of various factors. Since the cell cycle in multicellular eukaryotes responds to multiple extracellular mitogenic cues, its study in higher forms of life becomes all the more important. One such factor regulating cell cycle progression in plants is sugar signalling. Because the growth of organs depends on both cell growth and proliferation, sugars sensing and signalling are key control points linking sugar perception to regulation of downstream factors which facilitate these key developmental transitions. However, the basis of cell cycle control via sugars is intricate and demands exploration. This review deals with the information on sugar and TOR-SnRK1 signalling and how they manoeuvre various events of the cell cycle to ensure proper growth and development.

Complex genetic interaction between glucose sensor HXK1 and E3 SUMO ligase SIZ1 in regulating plant morphogenesis.

Sugar signaling forms the basis of metabolic activities crucial for an organism to perform essential life activities. In plants, sugars like glucose, mediate a wide range of physiological responses ranging from seed germination to cell senescence. This has led to the elucidation of cell signaling pathways involving glucose and its counterparts and the mechanism of how these sugars take control over major hormonal pathways such as auxin, ethylene, abscisic acid and cytokinin in Arabidopsis. Plants use HXK1(Hexokinase) as a glucose sensor to modulate changes in photosynthetic gene expression in response to high glucose levels. Other proteins such as SIZ1, a major SUMO E3 ligase have recently been implicated in controlling sugar responses via transcriptional and translational regulation of a wide array of sugar metabolic genes. Here, we show that these two genes work antagonistically and are epistatic in controlling responsiveness toward high glucose conditions.

Peroneal Artery Pseudoaneurysm after Surgery for Non-union of Tibia: A Case Report with Review of Literature.

Introduction: Arterial pseudoaneurysm is a hematoma that is formed after damage to the arterial wall. We report a rare case of peroneal artery pseudoaneurysm after open reduction and internal fixation with interlocking nailing and partial fibulectomy for non-union for the right tibia in a 31-year-old male. The patient presented with a bleeding sinus over the leg swelling, and it was managed with an exploration of the pseudoaneurysm and ligation of the peroneal artery. Case Report: A 30-year-old male patient presented with a non-union tibia on the right side and had undergone plating of the tibia at another institute for a fracture of both bone legs approximately 18 months ago. The revision surgery was performed in which a previously inserted implant was removed and an interlocking nail was inserted, along with a partial fibulectomy. The post-operative period was uneventful. At 8 weeks after the second surgery, the patient came with a complaint of swelling at the outer aspect of the right leg. Computed tomography and angiography confirmed a peroneal artery pseudoaneurysm of 3.2 × 2.8 × 3.8 cm. Pseudoaneurysm was explored, and the artery was overrun with a Figure-8 stitches using a monofilamentous, and non-absorbable suture. Conclusion: This case report highlights the occurrence of pseudoaneurysm after an orthoapedic procedure such as a partial fibulectomy. A high level of clinical suspicion, proper imaging, and early endovascular or surgical intervention is recommended to prevent complications.

Genetics on early onset inflammatory bowel disease: An update.

Inflammatory bowel disease (IBD) is more common in adults than in children. Onset of IBD before 17 years of age is referred as pediatric onset IBD and is further categorized as very early onset IBD (VEO-IBD) for children who are diagnosed before 6 years of age, infantile IBD who had the disease before 2 years of age and neonatal onset IBD for children less than 28 days of life. Children presenting with early onset disease may have a monogenic basis. Knowledge and awareness of the clinical manifestations facilitates early evaluation and diagnosis. Next generation sequencing is helpful in making the genetic diagnosis. Treatment of childhood IBD is difficult; targeted therapies and hematopoietic stem cell transplantation form the mainstay. In this review we aim to summarize the genetic defects associated with IBD phenotype. We describe genetic location and functions of various genetic defect associated with VEO-IBD with their key clinical manifestations. We also provide clinical clues to suspect these conditions and approaches to the diagnosis of these disorders and suitable treatment options.