Microarray data on altered transcriptional program of Phgdh-deficient mouse embryonic fibroblasts caused by ʟ-serine...

Area of Science:

• Biochemistry and Molecular Biology
• Developmental Biology
• Genomics

Background:

• Inborn errors of metabolism, specifically L-serine deficiency, lead to severe intrauterine growth retardation and multi-organ malformations, particularly affecting the central nervous system.
• These deficiencies can result in perinatal or early postnatal lethality in both human and mouse models.
• Understanding the molecular mechanisms behind these growth-arrested phenotypes is crucial for potential therapeutic interventions.

Purpose of the Study:

• To elucidate the molecular mechanisms underlying the growth-arrested phenotypes associated with L-serine deficiency.
• To compare gene expression profiles in cells with and without L-serine to identify key regulatory pathways.

Main Methods:

• Comparison of gene expression profiles using microarray analysis.
• Utilized mouse embryonic fibroblasts deficient in 3-phosphoglycerate dehydrogenase (Phgdh), the rate-limiting enzyme in de novo L-serine synthesis.
• Experimental conditions involved both L-serine-depleted and L-serine-supplemented media.

Main Results:

• Gene expression profiles were analyzed to identify molecular differences between L-serine-depleted and supplemented conditions.
• The study identified specific genes and pathways affected by the deficiency in de novo serine synthesis.
• Data are publicly available on Gene Expression Omnibus (GEO: GSE55687) for further research.

Conclusions:

• The study provides insights into the molecular basis of developmental defects caused by L-serine deficiency.
• Identifying affected gene expression patterns can pave the way for understanding the complex pathophysiology of serine deficiency disorders.
• The comprehensive gene expression data serves as a valuable resource for the scientific community studying serine metabolism and developmental biology.