Paolo Forni
University at Albany, NY·Neuroscience
Puberty and fertility depend on a small group of brain cells called GnRH-1 neurons. These neurons release the hormone that drives the reproductive system.
- Fields
Neuroscience
Genetics
Biology
- Topics
GnRH-1 neurons
gonadotropin-releasing hormone
neuronal migration
- Grants
- 2 known grants, through Oct 2029
What they work on
- Trace terminal nerve development in mice with genetic labeling and imaging to test whether GnRH-1 neurons migrate to the hypothalamus along this nerve and whether it is needed to form the olfactory bulbs.
- Use single-cell sequencing and human genomic data to define the genetic identity of terminal nerve neurons, and test whether Kallmann syndrome and nIHH genes act directly within them to disrupt GnRH-1 migration.
- Determine how different doses of Gli3, a transcription factor linked to Kallmann syndrome, affect terminal nerve development and gene expression in mice.
- Identify Gli3 target genes in the developing nose and the signals that form olfactory ensheathing cells, using CUT&RUN to map DNA binding, single-cell transcriptomics and bioinformatics.
More about the research
Surprisingly, they are born in the embryo's nose. From there they must migrate into the brain and settle in the hypothalamus, the brain region that controls the pituitary gland's hormone release. When this journey goes wrong, people can develop hypogonadotropic hypogonadism (HH). People with HH have delayed or absent puberty and are infertile. In Kallmann syndrome (KS), HH also comes with a reduced sense of smell. In normosmic idiopathic HH (nIHH), smell is normal. The lab studies the developing nose and its nerves to learn how this migration is built and how disease genes disrupt it.
Why it matters
Kallmann syndrome and normosmic idiopathic hypogonadotropic hypogonadism cause absent or delayed puberty and infertility. Identifying how mutated genes, including Gli3, disrupt the terminal nerve, olfactory ensheathing cells and GnRH-1 neuron migration could improve diagnosis of these conditions. It could also inform new approaches to treating hypogonadotropic hypogonadism and restoring fertility.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Molecular Mechanisms Underlying Terminal Nerve Development, GnRH-1 Neuronal Migration, and Olfactory Bulb Formation in Normal and Pathological Conditions
NIH · Nov 2024 – Oct 2029
Understanding the role of the transcription factor Gli3 in Kallmann syndrome and normosmic forms of idiopathic hypogonadotropic hypogonadism
NIH · Mar 2019 – Apr 2029
Closest labs
Aleisha Moore
Kent State University at Kent, OH·Neuroscience
Test whether estradiol and progesterone fail to suppress KNDy neuron activity in prenatally androgenized PCOS model mice, using in vivo calcium imaging of individual neurons in freely behaving animals alongside LH pulse measurements.
Bradley Goldstein
Duke University, NC·Neuroscience
Map the axes of gene-expression variation across human olfactory sensory neurons by single-cell RNA sequencing of nasal biopsies from people with normal smell and from people with objectively measured smell loss.
Eran Andrechek
Michigan State University, MI·Genetics
Characterize mammary gland defects in mice lacking E2F5 only in mammary epithelial cells, including duct extension during puberty, alveolar development and involution.
The school
University at Albany: 15 labs on PI Pages, $472M a year on research, 144 research doctorates a year.
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