The survival of species requires healthy function of oocytes. Excess stiffness of the ovarian microenvironment can cause infertility in humans and mice, though the underlying mechanisms are not clear. We recently found that loss of a poorly understood, highly conserved protein, Nuclear Envelope Membrane Protein 1 (NEMP1), is required for fertility in a wide-range of organisms (worms, flies, fish and mice). We also showed NEMP1 promotes nuclear envelope stiffness. Now we show  that loss of Nemp1 is required for survival on stiff surfaces and that YAP, the mechanosensitive transcriptional co-activator of the Hippo pathway, is sensitive to Nemp1 levels. Nemp1 is also required for YAP responses to diverse mechanical forces such as cell stretching.   Nemp1 contains an Intrinsically Disordered Region (IDR), and forms condensates in oocytes. Our preliminary data indicate this IDR can mediate phase transitions needed for condensate formation in oocytes.  Furthermore, Nemp1 condensates are sensitive to mechanical stresses. Loss of Nemp1 leads to loss of chromatin condensation, and dramatic loss of HP1 and H3K9me2 without altering other chromatin marks.  These findings point to Nemp1 a novel mechanism for nuclear sensing of stress that is critical for metazoan fertility.