About

Michael C. Golding is associated with the Texas A&M College of Veterinary Medicine & Biomedical Sciences (VMBS), which is ranked as the No. 3 veterinary college in the United States and is recognized for its research in animal science and veterinary medicine. The college emphasizes a 'One Health' approach, integrating animal, human, and environmental health through cutting-edge basic and clinical research. Golding's work is aligned with the college's mission to support collaborations that translate discoveries into proactive solutions for health challenges affecting animals, humans, and the environment. The college also engages in innovative research, veterinary education, outreach, and emergency support services, reflecting a comprehensive commitment to advancing veterinary medicine and biomedical sciences.

Research topics

• Genetics
• Biology
• Medicine
• Physiology
• Andrology
• Internal medicine
• Neuroscience
• Bioinformatics

Selected publications

• Physiologic variation in sperm miRNAs tune embryonic gene regulatory programs and developmental outcomes

  bioRxiv (Cold Spring Harbor Laboratory) · 2026-03-06

  articleOpen access

  ABSTRACT Small RNAs delivered by sperm can transmit environmentally regulated, epigenetically inherited phenotypes to offspring, yet the mechanisms by which modest changes in sperm microRNA abundance overcome dilution within the much larger egg to influence embryonic development remain unresolved. Here, we show that physiologically relevant variation in individual sperm miRNAs is sufficient to quantitatively program embryonic gene expression and developmental outcomes. Using parthenogenetic and fertilized embryos, we show that as few as 200 molecules of miR-200c-3p or miR-465c-3p induces reproducible, dose-dependent gene expression responses across defined developmental windows. Parthenogenetic embryos faithfully recapitulate early miRNA-driven gene expression changes observed in fertilized embryos, validating their use for isolating early regulatory mechanisms. We further developed AGO2-REMORA, an RNA adenosine base editor fused to Argonaute2 to map miRNA–mRNA interactions in embryos, revealing that early mRNA repression reflects direct miRNA targeting, while transcriptional changes at later stages arise as secondary consequences of these initial interactions. Furthermore, we show that modest elevation of miR-200c-3p during early development is sufficient to induce transcriptional alterations through early development and produce craniofacial phenotypes in late-stage embryos, recapitulating features of fetal alcohol syndrome associated with paternal alcohol consumption. Together, these findings establish a generalizable framework by which small perturbations in sperm miRNA content quantitatively modulate early gene regulatory programs, triggering cascades that persist throughout development and influence offspring phenotype.

  PublisherDOI

• MassIVE MSV000100811 - Paternal NRF2 Deficiency and Alcohol Exposure Alter Germline RNAs with Convergent Effects on Male Offspring Placental Development and Mitochondrial Function

  California Digital Library · 2026-01-01

  datasetOpen access1st authorCorresponding
  OA PDFDOI

• Contrasting epigenetics of Ixodes scapularis populations

  Scientific Reports · 2025-10-09

  preprintOpen access

  Hard ticks are a source of public health concern, in part due to their ability to inhabit different environments. In the United States (US), blacklegged ticks (Ixodes scapularis Say), the primary vector of Lyme disease, exhibit various phenotypes depending on their geographic origin (i.e. northern and southern US ticks). Although genetics may partially explain how blacklegged tick populations acclimate to different environmental conditions across the US, epigenetics may also contribute to their success. Epigenetic mechanisms, such as DNA methylation, might modulate gene expression allowing for rapid adaptation. To gain insight into the potential contribution of DNA methylation, an Enzyme-Linked Immunosorbent Assay (ELISA) was utilized to evaluate differences in DNA methylation levels between blacklegged ticks collected from Minnesota (northern region) and Texas (southern region). DNA methylation profiles from both populations were characterized using bisulfite and nanopore sequencing. Our results revealed significant variability in global methylation levels between southern and northern tick populations, as well as highly variable relative expression of genes encoding DNA methyltransferases and demethylases. Overall, northern blacklegged ticks exhibit lower global DNA methylation levels than southern ticks. Basic proline-rich protein, zinc finger protein 501-like protein, and an uncharacterized protein LOC115333191 are among the genes that exhibit lower DNA methylation. Our findings revealed that blacklegged tick populations possess distinctive DNA methylation profiles, which may contribute to their phenotypic plasticity across the US. This study aims to pave the way for future research into the potential molecular mechanisms that allow ticks to successfully acclimatize to environmental changes.

  PublisherOA PDFDOI

• Enteral immunization with live bacteria reprograms innate immune cells and protects neonatal foals from pneumonia

  Scientific Reports · 2025-05-25 · 1 citations

  articleOpen access

  Using a horse foal model, we show that enteral immunization of newborn foals with Rhodococcus equi overcomes neonatal vaccination challenges by reprogramming innate immune responses, inducing R. equi-specific adaptive humoral and cell-mediated immune responses and protecting foals against experimental pneumonia challenge. Foals were immunized twice via gavage of R. equi (immunized group) or saline (control group) at ages 1 and 3 days. At age 28 days, all foals were challenged intrabronchially with R. equi. Post-challenge, all 5 immunized foals remained healthy, whereas 67% (4/6) of control foals developed clinical pneumonia. Immunized foals exhibit changes in the epigenetic profile of blood monocytes, > 1,000 differentially-expressed genes in neutrophils, higher concentrations of R. equi-specific IgG1 and IgG4/7, and a higher number of IFN-γ producing lymphocytes in response to R. equi stimulation indicating T helper type 1 response compared to control foals. Together, our data indicate that early life exposure to R. equi in the gastrointestinal tract can modulate innate immune responses, generate specific antibodies and cell-mediated immunity, and protect against pneumonia.

  PublisherOA PDFDOI

• Maternal, paternal, and dual-parental alcohol exposures result in both overlapping and distinct impacts on behavior in adolescent offspring

  Alcohol · 2025-01-22 · 4 citations

  articleSenior authorCorresponding
  PublisherDOI

• Paternal NRF2 Deficiency and Chronic Alcohol Exposure Drive a Convergent Germline Signaling Axis to Alter Offspring Development

  SSRN Electronic Journal · 2025-01-01

  preprintOpen accessSenior author
  PublisherDOI

• Therapy to Teratology: Chronic Paternal Antioxidant Supplementation Alters Offspring Placental Architecture and Craniofacial Morphogenesis in a Mouse Model

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-09-10

  preprintOpen accessSenior authorCorresponding

  Oxidative stress plays a significant role in regulating the mammalian epigenome, with emerging evidence suggesting imbalances in the cellular redox state trigger stress-responsive epigenetic modifications that drive various human diseases. However, it remains unclear whether, like worms, epigenetic changes caused by redox imbalance or mitochondrial stress can move through the mammalian germline, potentially affecting the health of future generations. Antioxidant therapies are commonly used to reduce oxidative damage and are widely employed in cases of male infertility, where high-dose supplementation is often recommended to enhance sperm quality and overall measures of male reproductive health. Interestingly, in non-stressed, ostensibly healthy males, recent research suggests that antioxidants may have a negative influence on sperm epigenetic markers, indicating a potential epigenetic liability. However, whether male antioxidant treatment can induce paternal effects on offspring growth and development remains unknown. Here, we employed micro-CT imaging and geometric morphometrics to determine whether chronic antioxidant supplementation in healthy male mice affects placental growth and craniofacial development in their offspring. Adult C57BL/6J male mice were given a six-week preconception regimen of N-acetyl-L-cysteine (NAC; 400 mg/kg/day) and selenium (0.04 mg/kg/day), which continued throughout breeding with treatment-naïve females. Although we observed modest alterations to the histological patterning of the female placenta, placental weights and efficiency remained unchanged. In contrast, we observed significant changes in facial shape and symmetry in both male and female offspring, with female offspring exhibiting significant reductions in eye spacing and head area. These changes occurred without any macro changes in paternal metabolic health, indicating that antioxidant-induced shifts in redox balance may disrupt developmental programming in the male germline independent of changes in overall health. Our findings emphasize the need for caution when using antioxidants as preconception interventions and broadly suggest that modulation of the paternal redox axis may result in altered developmental programming and teratogenic effects.

  PublisherOA PDFDOI

• Preconception Paternal Alcohol Consumption Elicits Postnatal Changes in Neural Retinas of the Offspring

  Investigative Ophthalmology & Visual Science · 2025-02-06

  articleOpen access

  Purpose: This study aims to determine the impact of preconception paternal alcohol consumption (PPAC) on retinal function and morphology in PPAC-offspring. Fetal alcohol spectrum disorder (FASD)-related ocular defects caused by maternal alcohol exposure has been well investigated, but the influence of PPAC on offspring eyes remains unknown. Methods: Adult C57BL/6J male mice were exposed to either 10% ethanol or water (control) for six weeks and bred to naïve females. Dark-adapted retinal light responses at two, four, and six months old were assessed using electroretinography (ERG) for the offspring born to PPAC and control males. The thicknesses of whole retinas and different retinal layers of the control and PPAC-offspring were analyzed at two and six months old. Results: Some PPAC-offspring had only one developed eye. ERG a- and b-wave amplitudes were reduced in PPAC-offspring compared to controls, with a more pronounced effect in females. PPAC had significant effects on inner retinal function. At two months old, there was a significant thinning of the retinal inner nuclear and inner plexiform layers in PPAC-offspring. At six months old, the retinal thickness and ERG amplitudes were similar between both treatment groups. Conclusions: This study provides pioneering evidence that PPAC contributes to FASD-related ocular defects including negative impacts on retinal light responses and retinal thinning in young adult offspring. Thus the adverse impact of paternal alcohol consumption prior to conception on their offspring (from childhood to early adulthood) should be considered as seriously as the maternal contribution to FASD.

  PublisherOA PDFDOI

• Therapy to teratology: chronic paternal antioxidant supplementation alters offspring placental architecture and craniofacial morphogenesis in a mouse model

  Frontiers in Cell and Developmental Biology · 2025-12-19

  articleOpen accessSenior authorCorresponding

  Oxidative stress is an important regulator of the mammalian epigenome, with redox imbalances triggering stress-responsive epigenetic modifications linked to various diseases. Accordingly, antioxidant therapies are commonly used to reduce oxidative damage and are widely employed in cases of male infertility. Interestingly, in ostensibly healthy males, recent research suggests that antioxidants may have a negative influence on sperm DNA methylation, indicating a potential epigenetic liability. However, whether male antioxidant treatment can induce paternal effects on offspring growth and development remains untested. Here, we employed micro-CT imaging and geometric morphometrics to determine whether chronic antioxidant supplementation in healthy male mice affects placental growth and craniofacial development in their offspring. Adult C57BL/6J male mice were given a six-week preconception regimen of N-acetyl-L-cysteine and selenium, then paired with treatment-naïve females. Although we observed sex-specific changes in the decidua and junctional zone, we did not detect changes in placental weight and efficiency. In contrast, we observed significant changes in facial shape in both male and female offspring, with female offspring exhibiting significant reductions in eye spacing and head area. These changes occurred without any macro changes in paternal metabolic health, indicating that alterations in developmental programming may occur independent of changes in overall health. Our findings highlight the need for caution in the indiscriminate use of antioxidants, showing that supplementation in healthy males is not harmless and that perturbing the paternal redox balance may alter developmental programming and induce teratogenic outcomes.

  PublisherOA PDFDOI

• Alterations in placental vascular formation in parental alcohol exposure

  Physiology · 2025-05-01

  article

  Introduction: Recent studies indicate that maternal and paternal alcohol use disrupts the formation of placental vasculature. This disruption leads to placental insufficiency and fetal growth restriction, thus negatively affecting long-term offspring health. However, our understanding of the nature of such disruptions in placental vascular development remains limited. Our objective in this study was to understand and quantify the alterations in the collagen network interwinding the vascular bed in the placenta caused by parental alcohol exposure. Methods: The animal study was approved by the Texas A&M University IACUC. All experiments were performed following IACUC guidelines and regulations. 90-day postnatal C57BL/6J mice were used. The mice were separated into four groups: maternal (MatExp), paternal (PatExp), dual parental (DualExp), and control. We exposed males to 10% w/v ethanol six weeks before conception, while we exposed females one week before conception and for the first ten days of pregnancy. We used a 2x2 factorial experimental design to compare the placenta of offspring across groups. We examined placental development (n=35 placenta) on gestational day 16.5 using histological analysis, stained with Picro Sirius Red stain (Control n=5; MatExp n=13; PatExp n=10, DualExp n=7). The collagen portion of the images was isolated and analyzed to determine collagen fiber content and orientation. Statistical analysis was performed using one-way ANOVA with Tukey's correction for multiple comparisons. Significance was accepted at p<0.05. Results: Histological analysis indicated that collagen content decreased significantly in the MatExp and DualExp groups. (control: 59±7.9%; MatExp: 48±7.9% with p=0.0117 vs. control; PatExp: 53.7±9.7%; DualExp: 47.8±5.9% with p=0.0469 vs. control). In addition, collagen fiber spread, defined as the standard deviation in the collagen fiber orientation, increased in the MatExp group, but the change was less notable in the other two groups (control: 12±3.8°; MatExp: 23.6±6.5° with p=0.0826 vs. control; PatExp: 19.3±8.4°; DualExp: 18.9±5.9°). Conclusions: Alcohol-induced disorganization of the connective tissue supporting placental vasculature could indicate a significant disruption in placental blood supply, leading to placental dysfunction. Further investigation is required to elucidate the effects of the disorganized vasculature on placental function. This work was supported by the National Institutes of Health R00HL138288 to R.A. This abstract was presented at the American Physiology Summit 2025 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.

  PublisherDOI

Recent grants

• Altered genomic imprinting as a basis for FASD placental growth defects

  NIH · $371k · 2014–2017

• HERITABLE, EPIGENETIC EFFECTS OF PATERNAL ALCOHOL USE ON FASD PHENOTYPES

  NIH · $2.3M · 2026–2031

• NIH Grant R03AA020129

  NIH · $136k · 2013

Frequent coauthors

• Mellissa R.W. Mann

  Ottawa Hospital Research Institute

  24 shared

• Gregory J. Hannon

  Cancer Research UK

  23 shared

• Kara N. Thomas

  Texas A&M University

  18 shared

• Charles R. Long

  Texas A&M University

  18 shared

• José M. Silva

  17 shared

• Kenneth Chang

  16 shared

• Krista Marran

  NeuroMetrix (United States)

  16 shared

• Mark Westhusin

  16 shared

Education

• Post Doctoral Fellowship, Obstetrics & Gynecology

  University of Western Ontario Faculty of Science

  2009

• Post-Doctoral Fellow, Hannon Lab

  Cold Spring Harbor Laboratory

  2006

• PhD., Physiology

  Texas A&M University

  2003

• Honors BSc., Genetics

  University of Western Ontario Department of Biology

  2000