Target Audience

Des Moines University faculty, staff, and students.

Purpose

Although early paradigms for regulation of gene expression focused almost exclusively on transcription factor binding and recruitment of the RNA polymerase, we now know that gene expression levels can be exquisitely calibrated by chromatin structure and nuclear architectural influences.  And although histone modifications were first described as a "code" linked to "active" or "silent" chromatin states, work in my lab and others are revealing how these marks play a much more dynamic role in modulating gene function and chromosome behavior.  In this presentation the speaker will propose a model for enzymatic and non-enzymatic mechanisms by which the JIL-1 H3S10 kinase influences chromatin structure and chromosome architectural organization, and discuss developmental and physiological consequences of JIL-1 dysfunction.

Learning Objectives

• Distinguish how histone H3 modifications impact chromatin structure to promote open (euchromatic) or closed (heterochromatic) structure and its impact on gene expression. (Comprehension)
• Compare and contrast how the H3S10 JIL-1 kinase regulates chromatin structure/gene activity through enzymatic and non-enzymatic mechanisms (Analysis).
• Predict potential impacts on development/physiological function when the H3K9me2/S10ph marking system is dysfunctional.  (Synthesis).