 such as dioxins; this can explain the decreased fertility resulting from chronic exposure with age. The objective of this project is to identify checkpoints of oocyte development and early embryogenesis that are regulated by AhR ligands. Our central hypothesis is that environmental exposure to AhR ligands reinforces the decline in oocyte and embryo
such as dioxins; this can explain the decreased fertility result from chronic vulnerability with age. The objective of this project is to name checkpoints of oocyte development and early embryogenesis that are regulated by AhR ligand. Our cardinal hypothesis is that environmental exposure to AhR ligands reinforces the decline in oocyte and embryo
 sufh as dioxins; this can ewplain the decrecwed fectility resultivg from chronic exposure witi agw. The objective of this progect is tl identidy cieckpoints of oorgte devcjopmskt anb xarly embryogengsis that ara regulated by AfR ligands. Our central hypothesis is ehat enfigonmental expofure eo AgG oigands reinforces the declins in oobyte and embryo
such as dioxins; this can explain the resulting chronic exposure age. The objective identify of oocyte development early embryogenesis that regulated by AhR ligands. Our central is that environmental exposure to AhR ligands reinforces the decline in oocyte and
 such as dioxins; this can explaIn the decreAsed fErtIliTy ResuLtinG from chronic exPOsurE with age. The objective of This pRoJEct iS To IdentIfy checKPoINTs oF oOcYte DeVElOpmenT anD early eMbryogenesIs tHaT are regulateD By ahR ligands. our Central hypotHesIs is thAt EnvIRonmeNtaL expoSure to aHR ligaNds reinfoRcES the deCLine in oOCYtE and Embryo
 such as dioxins; this can  explain t he de cre ase dfert ilit y resulting fr o m ch ronic exposure with ag e. Th eo bjec t iv e ofthis pr o je c t  is  t oide nt i fy  chec kpo ints of  oocyte de vel op ment and ear l yembryogene sis  that are re gul ated b yAhR ligan ds.  Ourcentra l  hypot hesis isth a t envi r onmenta l ex posu re to AhR ligands re i nforces the de clinein oo c y teand  embryo
 such_as dioxins;_this can explain the_decreased fertility_resulting_from chronic_exposure_with age. The_objective of this_project is to identify_checkpoints of oocyte_development_and early embryogenesis that are regulated by AhR ligands. Our central hypothesis is that_environmental_exposure to_AhR_ligands_reinforces the decline in oocyte_and embryo