# REGULATION OF INTESTINAL DEVELOPMENT

> **NIH NIH R37** · BAYLOR COLLEGE OF MEDICINE · 1994 · $316,140

## Abstract

The overall goals of these studies are to gain an understanding of the
molecular and cellular biology of intestinal development and the roles of
glucocorticoids (GC) in the ontogenic process.  It appears that GC have
two distinct actions on the developing intestine:  early effects wherein
they advance the timing of initiation of enzymic changes, and late
effects, wherein they control only the rate of change.  Each of these
actions could potentially be exerted at the transcriptional level or at
any post-transcriptional level (e.g., message stabilization, translation
of post-translational processing).  Moreover, these effect of GC could
involve either the proliferating crypt epithelial cells, the
differentiating villus cells, or the underlying mesenchymal cells.  In
Specific Aims #1 and #2, sucrase/isomaltase (SI) will be used as a
developmental marker to investigate the molecular and cellular site of
both early and late effects of GC.  These studies, together with Specific
Aim #3, are also designed to distinguish between two general models that
have been proposed for intestinal development.  In Specific Aims #4 and
#5 the hope is to generate potentially powerful tools for subsequent
studies of this ontogenic process.  The details of the five Specific Aims
are as follows:  1. To determine whether critical features of rat
intestinal development previously deduced from measurements of sucrase
enzyme activity represent control at the level of mRNA accumulation.
specifically, to investigate; a) whether early effects of GC on SI mRNA
are mediated via crypt cells; b) whether SI mRNA concentrations display
increasing responsiveness to GC during the first two postnatal weeks; c)
whether SI mRNA concentrations cease responding to GC on approximately
day 18; d) the precise time course of enhanced expression of SI mRNA
following GC administration during the first two postnatal weeks.  2.  To
use sucrase enzyme activity and quantitation of Si mRNA to determine
whether: a) "late" effects of GC are due to action at the level of the
crypt or the villus; b) the timing of loss of GC responsiveness is
delayed by adrenalectomy and accelerated by administration of GC.  3.  To
identify regulatory gene products (RGPs) of GC action on the small
intestine by screening of an intestinal cDNA library with appropriately
subtracted probes, and to use the clones thus obtained as probes to
determine:  a) whether RGPs elicited by GC on immature intestine also
appear during normal and GC-independent development; b) the cellular site
(crypt vs. villus; epithelium vs. mesenchyme) of appearance of RGPs.  4.
To systematically screen a number of inbred and wild strains of mice to
identify one in which intestinal development is either delayed or
accelerated.  If such a strain is identified, it would be used in a
subsequent grant period to complement the data generated from above
studies by investigating the molecular genetics of intestinal
development.  5.  To isolate and characterize t...

## Key facts

- **NIH application ID:** 2197065
- **Project number:** 4R37HD014094-16
- **Recipient organization:** BAYLOR COLLEGE OF MEDICINE
- **SAM.gov UEI:** FXKMA43NTV21
- **Principal Investigator:** SUSAN J. HENNING
- **Activity code:** R37 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1994
- **Award amount:** $316,140
- **Award type:** 4N
- **Project period:** 1979-09-01 → 1999-03-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/2197065

## Citation

> US National Institutes of Health, RePORTER application 2197065, REGULATION OF INTESTINAL DEVELOPMENT (4R37HD014094-16). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/2197065. Licensed CC0.

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