Cyanobacteria are a promising photosynthetic chassis to produce biofuels, biochemicals, and pharmaceuticals at the expense of CO and light energy. Glycogen accumulation represents a universal carbon sink mechanism among cyanobacteria, storing excess carbon and energy from photosynthesis and may compete with product synthesis. Therefore, the glycogen synthesis pathway is often targeted to increase cyanobacterial production of desired carbon-based products. However, these manipulations caused severe physiological and metabolic impairments and often failed to optimize the overall performance of photosynthetic production. Here, in this work, we explored to mobilize the glycogen storage by strengthening glycogen degradation activities. In PCC 7942, we manipulated the abundances of glycogen phosphorylase (GlgP) with a theophylline dose-responsive riboswitch approach, which holds control over the cyanobacterial glycogen degradation process and successfully regulated the glycogen contents in the recombinant strain. Taking sucrose synthesis as a model, we explored the effects of enhanced glycogen degradation on sucrose production and glycogen storage. It is confirmed that under non-hypersaline conditions, the overexpressed facilitated the effective mobilization of glycogen storage and resulted in increased secretory sucrose production. The findings in this work provided fresh insights into the area of cyanobacteria glycogen metabolism engineering and would inspire the development of novel metabolic engineering approaches for efficient photosynthetic biosynthesis.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9284946PMC
http://dx.doi.org/10.3389/fbioe.2022.925311DOI Listing

Publication Analysis

Top Keywords

glycogen storage
16
glycogen
13
glycogen degradation
12
glycogen phosphorylase
8
pcc 7942
8
mobilize glycogen
8
sucrose synthesis
8
sucrose production
8
manipulating expression
4
expression glycogen
4

Similar Publications

Background: Pompe disease is a rare genetic disorder caused by a deficiency of the enzyme acid alpha-glucosidase. This condition leads to muscle weakness, respiratory problems, and heart abnormalities in affected individuals.

Methods: The aim of the study is to share our experience through cross sectional study of patients with infantile-onset Pompe disease (IOPD) with different genetic variations, resulting in diverse clinical presentations.

View Article and Find Full Text PDF

Homozygous missense variant in causes early-onset neurodegeneration, leukoencephalopathy and autoinflammation.

J Med Genet

January 2025

Division of Clinical and Metabolic Genetics, Department of Paediatrics, The Hospital for Sick Children, University of Toronto, Toronto, Ontario, Canada

Biallelic pathogenic variants in cause a fatal autosomal recessive multisystem disorder characterized by recurrent autoinflammation, hypomyelination, progressive neurodegeneration, microcephaly, failure to thrive, liver dysfunction, respiratory chain defects and accumulation of glycogen in skeletal muscle. No missense variants in have been reported to date.We report a 6-year-old boy with microcephaly, global developmental delays, lower limb spasticity with hyperreflexia, epilepsy, abnormal brain MRI, failure to thrive, recurrent fevers and transaminitis.

View Article and Find Full Text PDF

Structural insights into glucose-6-phosphate recognition and hydrolysis by human G6PC1.

Proc Natl Acad Sci U S A

January 2025

Beijing National Laboratory for Condensed Matter Physics, Laboratory of Soft Matter Physics, Institute of Physics, Chinese Academy of Sciences, Beijing 100190, China.

The glucose-6-phosphatase (G6Pase) is an integral membrane protein that catalyzes the hydrolysis of glucose-6-phosphate (G6P) in the endoplasmic reticulum lumen and plays a vital role in glucose homeostasis. Dysregulation or genetic mutations of G6Pase are associated with diabetes and glycogen storage disease 1a (GSD-1a). Studies have characterized the biophysical and biochemical properties of G6Pase; however, the structure and substrate recognition mechanism of G6Pase remain unclear.

View Article and Find Full Text PDF

Glycogen storage disease type IV (GSD IV) is a rare disease caused by a defect in glycogen branching enzyme 1 (GBE1), which played a crucial role in glycogen branching. GSD IV occurs once in approximately 1 in every 760,000 to 960,000 live births and is inherited in an autosomal recessive pattern. Early diagnosis of GSD IV is challenging due to non-specific symptoms, such as liver and spleen enlargement, which can overlap with other hematologic and hepatobiliary disorders.

View Article and Find Full Text PDF

Advanced 3D bioprinted liver models with human-induced hepatocytes for personalized toxicity screening.

J Tissue Eng

January 2025

Engineering Research Center of Pulmonary and Critical Care Medicine Technology and Device (Ministry of Education), Tianjin Institutes of Health Science, Institute of Biomedical Engineering, Chinese Academy of Medical Sciences & Peking Union Medical College, Tianjin, China.

The development of advanced models for assessing liver toxicity and drug responses is crucial for personalized medicine and preclinical drug development. 3D bioprinting technology provides opportunities to create human liver models that are suitable for conducting high-throughput screening for liver toxicity. In this study, we fabricated a humanized liver model using human-induced hepatocytes (hiHeps) derived from human fibroblasts via a rapid and efficient reprogramming process.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!