Biomedical subjects

Martina Rembold

Publications and source records attributed to Martina Rembold.

5 recordsLinked to original sources

PubMed2006

Individual cell migration serves as the driving force for optic vesicle evagination.

The cellular mechanisms underlying organ formation are largely unknown. We visualized early vertebrate eye morphogenesis at single-cell resolution by in vivo imaging in medaka (Oryzias latipes). Before optic vesicle evagination, retinal progenitor cells (RPCs) modulate their convergence in a fate-specific manner. Presumptive forebrain cells converge toward the midline, whereas medial RPCs remain stationary, predetermining the site of evagination. Subsequent optic vesicle evagination is driven by the active migration of individual RPCs. The analysis of mutants demonstrated that the retina-specific transcription factor rx3 determines the convergence and migration behaviors of RPCs. Hence, the migration of individual cells mediates essential steps of organ morphogenesis.

Animals↗

PubMed2005

Medial floor plate formation in zebrafish consists of two phases and requires trunk-derived Midkine-a.

The medial floor plate (MFP) organizes the specification of neurons and outgrowth of axons in the ventral spinal cord of vertebrates. We show that the growth factor Midkine-a, expressed in the paraxial mesoderm, is required for formation of the MFP in zebrafish. Our epistatic analyses demonstrate that development of MFP comprises two independent sequential phases. Following initial MFP induction in the gastrula organizer, Midkine-a regulates allocation of MFP cells during subsequent development. Thus in zebrafish, trunk-derived signals are required for complete MFP formation from a common pool of organizer-derived midline precursor cells.

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PubMed2004

Mutations affecting retina development in Medaka.

In a large scale mutagenesis screen of Medaka we identified 60 recessive zygotic mutations that affect retina development. Based on the onset and type of phenotypic abnormalities, the mutants were grouped into five categories: the first includes 11 mutants that are affected in neural plate and optic vesicle formation. The second group comprises 15 mutants that are impaired in optic vesicle growth. The third group includes 18 mutants that are affected in optic cup development. The fourth group contains 13 mutants with defects in retinal differentiation. 12 of these have smaller eyes, whereas one mutation results in enlarged eyes. The fifth group consists of three mutants with defects in retinal pigmentation. The collection of mutants will be used to address the molecular genetic mechanisms underlying vertebrate eye formation.

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PubMed2004

In vivo time-lapse imaging in medaka--n-heptanol blocks contractile rhythmical movements.

Medaka is an ideal model system for developmental studies as it combines the advantages of powerful genetics and classical embryology. Due to the accessibility, transparency and fast development, embryogenesis and morphogenesis can be followed in vivo. Microscopic time-lapse imaging, however, requires the immobilization of the object to be observed. In medaka rhythmical contractile movements of the blastoderm during early development hampered time-lapse studies, as they cause the embryo to rotate vividly. Here we show that the contractile movements can be reduced by continuous treatment with the gap-junction uncoupling agent n-heptanol up to the 12-somite stage (stage 23) without interfering with development. This allows for the first time to perform high-resolution time-lapse studies in medaka.

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PubMed2002

Essential function of histone deacetylase 1 in proliferation control and CDK inhibitor repression.

Histone deacetylases (HDACs) modulate chromatin structure and transcription, but little is known about their function in mammalian development. HDAC1 was implicated previously in the repression of genes required for cell proliferation and differentiation. Here we show that targeted disruption of both HDAC1 alleles results in embryonic lethality before E10.5 due to severe proliferation defects and retardation in development. HDAC1-deficient embryonic stem cells show reduced proliferation rates, which correlate with decreased cyclin-associated kinase activities and elevated levels of the cyclin-dependent kinase inhibitors p21(WAF1/CIP1) and p27(KIP1). Similarly, expression of p21 and p27 is up-regulated in HDAC1-null embryos. In addition, loss of HDAC1 leads to significantly reduced overall deacetylase activity, hyperacetylation of a subset of histones H3 and H4 and concomitant changes in other histone modifications. The expression of HDAC2 and HDAC3 is induced in HDAC1-deficient cells, but cannot compensate for loss of the enzyme, suggesting a unique function for HDAC1. Our study provides the first evidence that a histone deacetylase is essential for unrestricted cell proliferation by repressing the expression of selective cell cycle inhibitors.

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