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A study was conducted to evaluate the effect of heat stress on the expression pattern of reproduction related genes in Malabari breed of goat. The study was conducted during 45 days using twelve 10 months to one year old Malabari goats. The goats were randomly allocated into two groups: MC (n = 6; Malabari control) and MHS (n = 6; Malabari heat stress). Goats were stall-fed with a diet composed of 60% roughage and 40% concentrate. All animals had access to ad-libitum feed and water and they were fed and watered individually. The MC goats were placed in the shaded pens while MHS goats were exposed to heat stress in outside environment between 10.00 h and 16.00 h. At the end of study period, all 12 animals were slaughtered and their uterus tissues were collected for gene expression and histopathological studies. The temperature humidity index (THI) inside shed (74.9) proved that the animals were not stressed while in the outside environment (86.5) the animals were extremely distressed. Heat stress significantly (P <0.05) influenced the expression patterns of follicle stimulating hormone receptor (FSHR), luteinizing hormone receptor (LHR), estrogen receptor alpha (ESTR alpha), prostaglandin F2 alpha (PGF2 alpha) and cyclooxygenase-2 (COX-2). However, prostaglandin E2 (PGE2) did not differed between the groups. Further, a strong positive correlation (P < 0.01) was established for THI with both FSHR gene expression. A negative correlation was also established between THI and ESTR alpha (P < 0.01), PGF2 alpha (P < 0.01), PGE2 (P < 0.05) genes. However, heat stress did not influence the expression patterns of LHR; COX-2 genes. The histopathological section of uterine epithelial cells showed degenerative changes (P < 0.05) with less differentiation in MHS group as compared to MC group. The results from the study clearly indicated that heat stress was able to alter the reproductive activity related gene expressions at uterine level and this could be an indication of reduced reproductive efficiency in Malabari goats. (C) 2019 Elsevier Inc. All rights reserved.